CN116497117A - Application of MFSD2A as marker in preparation, screening or treatment of gastric cancer drugs - Google Patents
Application of MFSD2A as marker in preparation, screening or treatment of gastric cancer drugs Download PDFInfo
- Publication number
- CN116497117A CN116497117A CN202211147524.4A CN202211147524A CN116497117A CN 116497117 A CN116497117 A CN 116497117A CN 202211147524 A CN202211147524 A CN 202211147524A CN 116497117 A CN116497117 A CN 116497117A
- Authority
- CN
- China
- Prior art keywords
- gastric cancer
- mfsd2a
- marker
- expression
- gene
- Prior art date
- Legal status (The legal status is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the status listed.)
- Pending
Links
- 208000005718 Stomach Neoplasms Diseases 0.000 title claims abstract description 91
- 206010017758 gastric cancer Diseases 0.000 title claims abstract description 91
- 201000011549 stomach cancer Diseases 0.000 title claims abstract description 91
- 101001125170 Homo sapiens Sodium-dependent lysophosphatidylcholine symporter 1 Proteins 0.000 title claims abstract description 89
- 102100029462 Sodium-dependent lysophosphatidylcholine symporter 1 Human genes 0.000 title claims abstract description 89
- 238000012216 screening Methods 0.000 title claims abstract description 12
- 239000003550 marker Substances 0.000 title claims abstract description 10
- 238000002360 preparation method Methods 0.000 title claims abstract description 7
- 238000011282 treatment Methods 0.000 title abstract description 7
- 239000003560 cancer drug Substances 0.000 title description 3
- 230000014509 gene expression Effects 0.000 claims abstract description 36
- 239000000439 tumor marker Substances 0.000 claims abstract description 15
- 101100080108 Homo sapiens MFSD2A gene Proteins 0.000 claims abstract description 14
- 239000003814 drug Substances 0.000 claims abstract description 10
- 229940079593 drug Drugs 0.000 claims abstract description 6
- 108020004459 Small interfering RNA Proteins 0.000 claims description 12
- 108090000623 proteins and genes Proteins 0.000 claims description 11
- 150000003180 prostaglandins Chemical class 0.000 claims description 10
- 239000003795 chemical substances by application Substances 0.000 claims description 6
- 239000003153 chemical reaction reagent Substances 0.000 claims description 4
- 238000003745 diagnosis Methods 0.000 claims description 4
- 230000028327 secretion Effects 0.000 claims description 4
- 208000000461 Esophageal Neoplasms Diseases 0.000 claims description 2
- 206010030155 Oesophageal carcinoma Diseases 0.000 claims description 2
- 201000004101 esophageal cancer Diseases 0.000 claims description 2
- 239000013642 negative control Substances 0.000 claims description 2
- 239000013641 positive control Substances 0.000 claims description 2
- 238000012360 testing method Methods 0.000 claims description 2
- 238000002474 experimental method Methods 0.000 abstract description 14
- 238000010276 construction Methods 0.000 abstract 1
- 230000009545 invasion Effects 0.000 abstract 1
- 210000004027 cell Anatomy 0.000 description 57
- 230000000694 effects Effects 0.000 description 16
- 230000002018 overexpression Effects 0.000 description 13
- YZXBAPSDXZZRGB-DOFZRALJSA-N arachidonic acid Chemical compound CCCCC\C=C/C\C=C/C\C=C/C\C=C/CCCC(O)=O YZXBAPSDXZZRGB-DOFZRALJSA-N 0.000 description 12
- 206010028980 Neoplasm Diseases 0.000 description 11
- 102000002574 p38 Mitogen-Activated Protein Kinases Human genes 0.000 description 11
- 102000004887 Transforming Growth Factor beta Human genes 0.000 description 9
- 108090001012 Transforming Growth Factor beta Proteins 0.000 description 9
- ZRKFYGHZFMAOKI-QMGMOQQFSA-N tgfbeta Chemical compound C([C@H](NC(=O)[C@H](C(C)C)NC(=O)CNC(=O)[C@H](CCC(O)=O)NC(=O)[C@H](CCCNC(N)=N)NC(=O)[C@H](CC(N)=O)NC(=O)[C@H](CC(C)C)NC(=O)[C@H]([C@@H](C)O)NC(=O)[C@H](CCC(O)=O)NC(=O)[C@H]([C@@H](C)O)NC(=O)[C@H](CC(C)C)NC(=O)CNC(=O)[C@H](C)NC(=O)[C@H](CO)NC(=O)[C@H](CCC(N)=O)NC(=O)[C@@H](NC(=O)[C@H](C)NC(=O)[C@H](C)NC(=O)[C@@H](NC(=O)[C@H](CC(C)C)NC(=O)[C@@H](N)CCSC)C(C)C)[C@@H](C)CC)C(=O)N[C@@H]([C@@H](C)O)C(=O)N[C@@H](C(C)C)C(=O)N[C@@H](CC=1C=CC=CC=1)C(=O)N[C@@H](C)C(=O)N1[C@@H](CCC1)C(=O)N[C@@H]([C@@H](C)O)C(=O)N[C@@H](CC(N)=O)C(=O)N[C@@H](CCC(O)=O)C(=O)N[C@@H](C)C(=O)N[C@@H](CC=1C=CC=CC=1)C(=O)N[C@@H](CCCNC(N)=N)C(=O)N[C@@H](C)C(=O)N[C@@H](CC(C)C)C(=O)N1[C@@H](CCC1)C(=O)N1[C@@H](CCC1)C(=O)N[C@@H](CCCNC(N)=N)C(=O)N[C@@H](CCC(O)=O)C(=O)N[C@@H](CCCNC(N)=N)C(=O)N[C@@H](CO)C(=O)N[C@@H](CCCNC(N)=N)C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CC(C)C)C(O)=O)C1=CC=C(O)C=C1 ZRKFYGHZFMAOKI-QMGMOQQFSA-N 0.000 description 9
- 210000001519 tissue Anatomy 0.000 description 9
- 230000010261 cell growth Effects 0.000 description 7
- 230000002401 inhibitory effect Effects 0.000 description 7
- 239000000047 product Substances 0.000 description 7
- 102000004169 proteins and genes Human genes 0.000 description 7
- 230000019491 signal transduction Effects 0.000 description 7
- RYCNUMLMNKHWPZ-SNVBAGLBSA-N 1-acetyl-sn-glycero-3-phosphocholine Chemical compound CC(=O)OC[C@@H](O)COP([O-])(=O)OCC[N+](C)(C)C RYCNUMLMNKHWPZ-SNVBAGLBSA-N 0.000 description 6
- 206010027476 Metastases Diseases 0.000 description 6
- 239000012826 P38 inhibitor Substances 0.000 description 6
- 102000046299 Transforming Growth Factor beta1 Human genes 0.000 description 6
- 101800002279 Transforming growth factor beta-1 Proteins 0.000 description 6
- 229940114079 arachidonic acid Drugs 0.000 description 6
- 235000021342 arachidonic acid Nutrition 0.000 description 6
- 230000015572 biosynthetic process Effects 0.000 description 6
- 238000001514 detection method Methods 0.000 description 6
- 238000001727 in vivo Methods 0.000 description 6
- 239000000463 material Substances 0.000 description 6
- 230000009401 metastasis Effects 0.000 description 6
- 230000004913 activation Effects 0.000 description 5
- 238000003786 synthesis reaction Methods 0.000 description 5
- 229940124638 COX inhibitor Drugs 0.000 description 4
- 238000002965 ELISA Methods 0.000 description 4
- 238000011529 RT qPCR Methods 0.000 description 4
- 239000012528 membrane Substances 0.000 description 4
- 230000004060 metabolic process Effects 0.000 description 4
- 239000003358 phospholipase A2 inhibitor Substances 0.000 description 4
- 238000011160 research Methods 0.000 description 4
- 238000010186 staining Methods 0.000 description 4
- 238000001890 transfection Methods 0.000 description 4
- 108091032973 (ribonucleotides)n+m Proteins 0.000 description 3
- 206010058467 Lung neoplasm malignant Diseases 0.000 description 3
- 239000002299 complementary DNA Substances 0.000 description 3
- 238000010586 diagram Methods 0.000 description 3
- 239000003112 inhibitor Substances 0.000 description 3
- 201000005202 lung cancer Diseases 0.000 description 3
- 208000020816 lung neoplasm Diseases 0.000 description 3
- 108010082117 matrigel Proteins 0.000 description 3
- 108091027963 non-coding RNA Proteins 0.000 description 3
- 102000042567 non-coding RNA Human genes 0.000 description 3
- 230000037361 pathway Effects 0.000 description 3
- 239000012096 transfection reagent Substances 0.000 description 3
- 230000009261 transgenic effect Effects 0.000 description 3
- 229920001817 Agar Polymers 0.000 description 2
- 102000004190 Enzymes Human genes 0.000 description 2
- 108090000790 Enzymes Proteins 0.000 description 2
- WZUVPPKBWHMQCE-UHFFFAOYSA-N Haematoxylin Chemical compound C12=CC(O)=C(O)C=C2CC2(O)C1C1=CC=C(O)C(O)=C1OC2 WZUVPPKBWHMQCE-UHFFFAOYSA-N 0.000 description 2
- 241000713666 Lentivirus Species 0.000 description 2
- 241000699670 Mus sp. Species 0.000 description 2
- 108091027967 Small hairpin RNA Proteins 0.000 description 2
- DBMJMQXJHONAFJ-UHFFFAOYSA-M Sodium laurylsulphate Chemical compound [Na+].CCCCCCCCCCCCOS([O-])(=O)=O DBMJMQXJHONAFJ-UHFFFAOYSA-M 0.000 description 2
- SXEHKFHPFVVDIR-UHFFFAOYSA-N [4-(4-hydrazinylphenyl)phenyl]hydrazine Chemical compound C1=CC(NN)=CC=C1C1=CC=C(NN)C=C1 SXEHKFHPFVVDIR-UHFFFAOYSA-N 0.000 description 2
- 239000000332 adrenergic beta-1 receptor antagonist Substances 0.000 description 2
- 239000008272 agar Substances 0.000 description 2
- 238000004458 analytical method Methods 0.000 description 2
- 201000011510 cancer Diseases 0.000 description 2
- 230000004709 cell invasion Effects 0.000 description 2
- 238000012512 characterization method Methods 0.000 description 2
- XEYBRNLFEZDVAW-ARSRFYASSA-N dinoprostone Chemical compound CCCCC[C@H](O)\C=C\[C@H]1[C@H](O)CC(=O)[C@@H]1C\C=C/CCCC(O)=O XEYBRNLFEZDVAW-ARSRFYASSA-N 0.000 description 2
- 229960002986 dinoprostone Drugs 0.000 description 2
- 230000009950 gastric cancer growth Effects 0.000 description 2
- 230000003834 intracellular effect Effects 0.000 description 2
- 230000037356 lipid metabolism Effects 0.000 description 2
- 230000007246 mechanism Effects 0.000 description 2
- 238000000034 method Methods 0.000 description 2
- 230000035772 mutation Effects 0.000 description 2
- 239000002953 phosphate buffered saline Substances 0.000 description 2
- XEYBRNLFEZDVAW-UHFFFAOYSA-N prostaglandin E2 Natural products CCCCCC(O)C=CC1C(O)CC(=O)C1CC=CCCCC(O)=O XEYBRNLFEZDVAW-UHFFFAOYSA-N 0.000 description 2
- -1 prostaglandin compound Chemical class 0.000 description 2
- 238000010839 reverse transcription Methods 0.000 description 2
- 230000002441 reversible effect Effects 0.000 description 2
- 238000012163 sequencing technique Methods 0.000 description 2
- 239000004055 small Interfering RNA Substances 0.000 description 2
- 229910001415 sodium ion Inorganic materials 0.000 description 2
- 230000004083 survival effect Effects 0.000 description 2
- 230000001225 therapeutic effect Effects 0.000 description 2
- 210000004881 tumor cell Anatomy 0.000 description 2
- 230000004614 tumor growth Effects 0.000 description 2
- 102100022089 Acyl-[acyl-carrier-protein] hydrolase Human genes 0.000 description 1
- 102100034540 Adenomatous polyposis coli protein Human genes 0.000 description 1
- 229920000936 Agarose Polymers 0.000 description 1
- 101100243447 Arabidopsis thaliana PER53 gene Proteins 0.000 description 1
- 102000008096 B7-H1 Antigen Human genes 0.000 description 1
- 108010074708 B7-H1 Antigen Proteins 0.000 description 1
- 208000003174 Brain Neoplasms Diseases 0.000 description 1
- 108010078791 Carrier Proteins Proteins 0.000 description 1
- 108091007854 Cdh1/Fizzy-related Proteins 0.000 description 1
- 102000038594 Cdh1/Fizzy-related Human genes 0.000 description 1
- 102100025064 Cellular tumor antigen p53 Human genes 0.000 description 1
- 102000007260 Deoxyribonuclease I Human genes 0.000 description 1
- 108010008532 Deoxyribonuclease I Proteins 0.000 description 1
- 239000006144 Dulbecco’s modified Eagle's medium Substances 0.000 description 1
- 230000037057 G1 phase arrest Effects 0.000 description 1
- 102100030708 GTPase KRas Human genes 0.000 description 1
- 101000824278 Homo sapiens Acyl-[acyl-carrier-protein] hydrolase Proteins 0.000 description 1
- 101000924577 Homo sapiens Adenomatous polyposis coli protein Proteins 0.000 description 1
- 101000584612 Homo sapiens GTPase KRas Proteins 0.000 description 1
- 101001012157 Homo sapiens Receptor tyrosine-protein kinase erbB-2 Proteins 0.000 description 1
- 108010001336 Horseradish Peroxidase Proteins 0.000 description 1
- DGAQECJNVWCQMB-PUAWFVPOSA-M Ilexoside XXIX Chemical compound C[C@@H]1CC[C@@]2(CC[C@@]3(C(=CC[C@H]4[C@]3(CC[C@@H]5[C@@]4(CC[C@@H](C5(C)C)OS(=O)(=O)[O-])C)C)[C@@H]2[C@]1(C)O)C)C(=O)O[C@H]6[C@@H]([C@H]([C@@H]([C@H](O6)CO)O)O)O.[Na+] DGAQECJNVWCQMB-PUAWFVPOSA-M 0.000 description 1
- 206010061218 Inflammation Diseases 0.000 description 1
- 208000007433 Lymphatic Metastasis Diseases 0.000 description 1
- 206010063916 Metastatic gastric cancer Diseases 0.000 description 1
- 241000699666 Mus <mouse, genus> Species 0.000 description 1
- 241000699660 Mus musculus Species 0.000 description 1
- 208000012902 Nervous system disease Diseases 0.000 description 1
- 241000283973 Oryctolagus cuniculus Species 0.000 description 1
- 102100030086 Receptor tyrosine-protein kinase erbB-2 Human genes 0.000 description 1
- 102000018120 Recombinases Human genes 0.000 description 1
- 108010091086 Recombinases Proteins 0.000 description 1
- 102000008078 Sterol Regulatory Element Binding Protein 1 Human genes 0.000 description 1
- 108010074436 Sterol Regulatory Element Binding Protein 1 Proteins 0.000 description 1
- 101150080074 TP53 gene Proteins 0.000 description 1
- 102000005789 Vascular Endothelial Growth Factors Human genes 0.000 description 1
- 108010019530 Vascular Endothelial Growth Factors Proteins 0.000 description 1
- 230000002159 abnormal effect Effects 0.000 description 1
- 230000000259 anti-tumor effect Effects 0.000 description 1
- 230000000840 anti-viral effect Effects 0.000 description 1
- 239000000427 antigen Substances 0.000 description 1
- 108091007433 antigens Proteins 0.000 description 1
- 102000036639 antigens Human genes 0.000 description 1
- 230000003305 autocrine Effects 0.000 description 1
- 230000009286 beneficial effect Effects 0.000 description 1
- 230000008901 benefit Effects 0.000 description 1
- 230000037396 body weight Effects 0.000 description 1
- 230000021164 cell adhesion Effects 0.000 description 1
- 230000012292 cell migration Effects 0.000 description 1
- 239000006285 cell suspension Substances 0.000 description 1
- 230000008859 change Effects 0.000 description 1
- 239000012295 chemical reaction liquid Substances 0.000 description 1
- 239000007979 citrate buffer Substances 0.000 description 1
- 238000003776 cleavage reaction Methods 0.000 description 1
- 150000001875 compounds Chemical class 0.000 description 1
- 239000012228 culture supernatant Substances 0.000 description 1
- 238000012258 culturing Methods 0.000 description 1
- 230000009089 cytolysis Effects 0.000 description 1
- 230000007547 defect Effects 0.000 description 1
- 230000001419 dependent effect Effects 0.000 description 1
- 238000011161 development Methods 0.000 description 1
- 230000018109 developmental process Effects 0.000 description 1
- 235000014113 dietary fatty acids Nutrition 0.000 description 1
- 238000007865 diluting Methods 0.000 description 1
- 238000010790 dilution Methods 0.000 description 1
- 239000012895 dilution Substances 0.000 description 1
- LOKCTEFSRHRXRJ-UHFFFAOYSA-I dipotassium trisodium dihydrogen phosphate hydrogen phosphate dichloride Chemical compound P(=O)(O)(O)[O-].[K+].P(=O)(O)([O-])[O-].[Na+].[Na+].[Cl-].[K+].[Cl-].[Na+] LOKCTEFSRHRXRJ-UHFFFAOYSA-I 0.000 description 1
- 238000013399 early diagnosis Methods 0.000 description 1
- 230000008030 elimination Effects 0.000 description 1
- 238000003379 elimination reaction Methods 0.000 description 1
- 230000013020 embryo development Effects 0.000 description 1
- 230000002708 enhancing effect Effects 0.000 description 1
- 239000013604 expression vector Substances 0.000 description 1
- 239000000194 fatty acid Substances 0.000 description 1
- 229930195729 fatty acid Natural products 0.000 description 1
- 150000004665 fatty acids Chemical class 0.000 description 1
- 230000002496 gastric effect Effects 0.000 description 1
- 239000003292 glue Substances 0.000 description 1
- 239000001963 growth medium Substances 0.000 description 1
- 230000000887 hydrating effect Effects 0.000 description 1
- 230000002055 immunohistochemical effect Effects 0.000 description 1
- 238000011532 immunohistochemical staining Methods 0.000 description 1
- 230000001506 immunosuppresive effect Effects 0.000 description 1
- 238000000338 in vitro Methods 0.000 description 1
- 208000015181 infectious disease Diseases 0.000 description 1
- 230000004054 inflammatory process Effects 0.000 description 1
- 230000002452 interceptive effect Effects 0.000 description 1
- 230000000670 limiting effect Effects 0.000 description 1
- 150000002632 lipids Chemical class 0.000 description 1
- 150000004668 long chain fatty acids Chemical class 0.000 description 1
- 238000004519 manufacturing process Methods 0.000 description 1
- 239000002609 medium Substances 0.000 description 1
- 230000006680 metabolic alteration Effects 0.000 description 1
- 230000011987 methylation Effects 0.000 description 1
- 238000007069 methylation reaction Methods 0.000 description 1
- 238000013508 migration Methods 0.000 description 1
- 230000004048 modification Effects 0.000 description 1
- 238000012986 modification Methods 0.000 description 1
- 230000007935 neutral effect Effects 0.000 description 1
- 238000011580 nude mouse model Methods 0.000 description 1
- 150000003904 phospholipids Chemical class 0.000 description 1
- 239000013612 plasmid Substances 0.000 description 1
- 238000010837 poor prognosis Methods 0.000 description 1
- 238000004393 prognosis Methods 0.000 description 1
- 230000001737 promoting effect Effects 0.000 description 1
- 102000005962 receptors Human genes 0.000 description 1
- 108020003175 receptors Proteins 0.000 description 1
- 230000002829 reductive effect Effects 0.000 description 1
- 230000022532 regulation of transcription, DNA-dependent Effects 0.000 description 1
- 238000004153 renaturation Methods 0.000 description 1
- 230000004044 response Effects 0.000 description 1
- 230000007017 scission Effects 0.000 description 1
- 238000007789 sealing Methods 0.000 description 1
- 230000011664 signaling Effects 0.000 description 1
- 239000011734 sodium Substances 0.000 description 1
- 229910052708 sodium Inorganic materials 0.000 description 1
- 239000000243 solution Substances 0.000 description 1
- 238000010254 subcutaneous injection Methods 0.000 description 1
- 239000007929 subcutaneous injection Substances 0.000 description 1
- 239000006228 supernatant Substances 0.000 description 1
- 230000008685 targeting Effects 0.000 description 1
- 231100000331 toxic Toxicity 0.000 description 1
- 230000002588 toxic effect Effects 0.000 description 1
- 238000012546 transfer Methods 0.000 description 1
- 108091005703 transmembrane proteins Proteins 0.000 description 1
- 102000035160 transmembrane proteins Human genes 0.000 description 1
- 230000032258 transport Effects 0.000 description 1
- 230000007723 transport mechanism Effects 0.000 description 1
- 230000009452 underexpressoin Effects 0.000 description 1
- 239000013598 vector Substances 0.000 description 1
- 238000005406 washing Methods 0.000 description 1
Classifications
-
- C—CHEMISTRY; METALLURGY
- C12—BIOCHEMISTRY; BEER; SPIRITS; WINE; VINEGAR; MICROBIOLOGY; ENZYMOLOGY; MUTATION OR GENETIC ENGINEERING
- C12Q—MEASURING OR TESTING PROCESSES INVOLVING ENZYMES, NUCLEIC ACIDS OR MICROORGANISMS; COMPOSITIONS OR TEST PAPERS THEREFOR; PROCESSES OF PREPARING SUCH COMPOSITIONS; CONDITION-RESPONSIVE CONTROL IN MICROBIOLOGICAL OR ENZYMOLOGICAL PROCESSES
- C12Q1/00—Measuring or testing processes involving enzymes, nucleic acids or microorganisms; Compositions therefor; Processes of preparing such compositions
- C12Q1/68—Measuring or testing processes involving enzymes, nucleic acids or microorganisms; Compositions therefor; Processes of preparing such compositions involving nucleic acids
- C12Q1/6876—Nucleic acid products used in the analysis of nucleic acids, e.g. primers or probes
- C12Q1/6883—Nucleic acid products used in the analysis of nucleic acids, e.g. primers or probes for diseases caused by alterations of genetic material
- C12Q1/6886—Nucleic acid products used in the analysis of nucleic acids, e.g. primers or probes for diseases caused by alterations of genetic material for cancer
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
- A61K38/00—Medicinal preparations containing peptides
- A61K38/16—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof
- A61K38/17—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof from animals; from humans
- A61K38/1703—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof from animals; from humans from vertebrates
- A61K38/1709—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof from animals; from humans from vertebrates from mammals
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
- A61K45/00—Medicinal preparations containing active ingredients not provided for in groups A61K31/00 - A61K41/00
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P35/00—Antineoplastic agents
-
- G—PHYSICS
- G01—MEASURING; TESTING
- G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
- G01N33/00—Investigating or analysing materials by specific methods not covered by groups G01N1/00 - G01N31/00
- G01N33/48—Biological material, e.g. blood, urine; Haemocytometers
- G01N33/50—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing
- G01N33/53—Immunoassay; Biospecific binding assay; Materials therefor
- G01N33/574—Immunoassay; Biospecific binding assay; Materials therefor for cancer
- G01N33/57407—Specifically defined cancers
- G01N33/57446—Specifically defined cancers of stomach or intestine
-
- G—PHYSICS
- G01—MEASURING; TESTING
- G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
- G01N33/00—Investigating or analysing materials by specific methods not covered by groups G01N1/00 - G01N31/00
- G01N33/48—Biological material, e.g. blood, urine; Haemocytometers
- G01N33/50—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing
- G01N33/53—Immunoassay; Biospecific binding assay; Materials therefor
- G01N33/574—Immunoassay; Biospecific binding assay; Materials therefor for cancer
- G01N33/57484—Immunoassay; Biospecific binding assay; Materials therefor for cancer involving compounds serving as markers for tumor, cancer, neoplasia, e.g. cellular determinants, receptors, heat shock/stress proteins, A-protein, oligosaccharides, metabolites
-
- C—CHEMISTRY; METALLURGY
- C12—BIOCHEMISTRY; BEER; SPIRITS; WINE; VINEGAR; MICROBIOLOGY; ENZYMOLOGY; MUTATION OR GENETIC ENGINEERING
- C12Q—MEASURING OR TESTING PROCESSES INVOLVING ENZYMES, NUCLEIC ACIDS OR MICROORGANISMS; COMPOSITIONS OR TEST PAPERS THEREFOR; PROCESSES OF PREPARING SUCH COMPOSITIONS; CONDITION-RESPONSIVE CONTROL IN MICROBIOLOGICAL OR ENZYMOLOGICAL PROCESSES
- C12Q2600/00—Oligonucleotides characterized by their use
- C12Q2600/136—Screening for pharmacological compounds
-
- C—CHEMISTRY; METALLURGY
- C12—BIOCHEMISTRY; BEER; SPIRITS; WINE; VINEGAR; MICROBIOLOGY; ENZYMOLOGY; MUTATION OR GENETIC ENGINEERING
- C12Q—MEASURING OR TESTING PROCESSES INVOLVING ENZYMES, NUCLEIC ACIDS OR MICROORGANISMS; COMPOSITIONS OR TEST PAPERS THEREFOR; PROCESSES OF PREPARING SUCH COMPOSITIONS; CONDITION-RESPONSIVE CONTROL IN MICROBIOLOGICAL OR ENZYMOLOGICAL PROCESSES
- C12Q2600/00—Oligonucleotides characterized by their use
- C12Q2600/158—Expression markers
-
- G—PHYSICS
- G01—MEASURING; TESTING
- G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
- G01N2333/00—Assays involving biological materials from specific organisms or of a specific nature
- G01N2333/435—Assays involving biological materials from specific organisms or of a specific nature from animals; from humans
- G01N2333/46—Assays involving biological materials from specific organisms or of a specific nature from animals; from humans from vertebrates
- G01N2333/47—Assays involving proteins of known structure or function as defined in the subgroups
-
- G—PHYSICS
- G01—MEASURING; TESTING
- G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
- G01N2500/00—Screening for compounds of potential therapeutic value
- G01N2500/04—Screening involving studying the effect of compounds C directly on molecule A (e.g. C are potential ligands for a receptor A, or potential substrates for an enzyme A)
Landscapes
- Health & Medical Sciences (AREA)
- Life Sciences & Earth Sciences (AREA)
- Chemical & Material Sciences (AREA)
- Engineering & Computer Science (AREA)
- Immunology (AREA)
- General Health & Medical Sciences (AREA)
- Molecular Biology (AREA)
- Medicinal Chemistry (AREA)
- Urology & Nephrology (AREA)
- Hematology (AREA)
- Analytical Chemistry (AREA)
- Proteomics, Peptides & Aminoacids (AREA)
- Biomedical Technology (AREA)
- Organic Chemistry (AREA)
- Pathology (AREA)
- Microbiology (AREA)
- Biotechnology (AREA)
- Animal Behavior & Ethology (AREA)
- Zoology (AREA)
- Biochemistry (AREA)
- Hospice & Palliative Care (AREA)
- Pharmacology & Pharmacy (AREA)
- Public Health (AREA)
- Physics & Mathematics (AREA)
- Cell Biology (AREA)
- Oncology (AREA)
- Veterinary Medicine (AREA)
- Bioinformatics & Cheminformatics (AREA)
- Epidemiology (AREA)
- General Physics & Mathematics (AREA)
- Genetics & Genomics (AREA)
- Food Science & Technology (AREA)
- Wood Science & Technology (AREA)
- Gastroenterology & Hepatology (AREA)
- General Engineering & Computer Science (AREA)
- Biophysics (AREA)
- Marine Sciences & Fisheries (AREA)
- Chemical Kinetics & Catalysis (AREA)
- General Chemical & Material Sciences (AREA)
- Nuclear Medicine, Radiotherapy & Molecular Imaging (AREA)
Abstract
The invention relates to the technical field of biological medicines, in particular to application of MFSD2A serving as a marker in preparation, screening or treatment of gastric cancer medicines, experiments show that MFSD2A is low in expression in gastric cancer tissues, the MFSD2A can inhibit growth and invasion of gastric cancer cells, and the MFSD2A gene or an expression product gastric cancer marker thereof is used as a gastric cancer marker according to the conclusion and applied to construction of a gastric cancer early screening model, preparation of products for diagnosing gastric cancer and preparation of medicines for preventing and treating gastric cancer.
Description
Technical Field
The invention relates to the technical field of biological medicines, in particular to application of MFSD2A serving as a marker in preparation, screening or treatment of gastric cancer drugs.
Background
The stomach cancer transfer mechanism is complex, and the stomach cancer can be generated and transferred due to the mutation of genes such as KRAS, P53, CDH1, APC and the like in stomach cancer cells. These genetic mutations tend to be present in only a fraction of patients. Metabolic alterations are a common property of tumor cells. Tumor cells can directly promote gastric cancer metastasis by enhancing sugar metabolism, and expression of lipid metabolism key enzymes SREBP1 and FASN are closely related to gastric cancer lymph node metastasis. In addition, with intensive research into long-chain non-coding RNAs, their important role in gastric cancer metastasis has also been discovered, and different types of long-chain non-coding RNAs can produce diametrically opposite roles. It follows that gastric cancer metastasis is a key factor affecting patient survival and therapeutic effect, and gastric cancer metastasis mechanism is still a major scientific problem to be solved in clinical and basic research.
Because of individual differences among different gastric cancer patients, the development of tumor-specific targets is a current research hotspot. The specific inhibitor can be used for patients with high-expression metastatic gastric cancer such as VEGF, PD-L1, HER2 and the like to improve the survival time of the patients to a certain extent. However, the clinical response rates of these specific inhibitors are generally low. So there are researchers targeting multiple markers simultaneously to improve the therapeutic effect of gastric cancer, however, this clearly increases the toxic side effects on patients. Thus, screening for new, more effective markers would help in the accurate treatment of cancer.
The main cofactor superfamily protein (MFSD 2A) is a sodium-dependent Lysophosphatidylcholine (LPC) transporter, whose structure is a transmembrane protein containing 12 alpha helices, whose main function is to transport LPC containing DHA and other long chain fatty acids, the transport mechanism of which is as follows: after Na ions are bound to the MFSD2A, LPC carries corresponding fatty acid to enter a phospholipid bilayer, and then the LPC moves transversely to be bound to the MFSD2A protein, at the moment, the protein undergoes conformational change, the opening to the outside of the membrane is changed into the opening to the inside of the membrane, na ions are released into cells, and LPC is transferred to the inner membrane of the cells. MFSD2A also plays an important role in the fields of embryo development, inflammation elimination, antiviral infection, nervous system diseases, and the like.
Currently, few reports are made about MFSD2A in tumors. In brain tumors, MFSD2A prevents cancer cell metastasis by restoring intracellular DHA metabolism. MFSD2A can induce phase G1 arrest of lung cancer cells, impairing cell adhesion and migration, and thereby inhibiting lung cancer cell growth. Meanwhile, lung cancer patients with abnormal MFSD2A methylation are found to have poor prognosis. From this, it can be seen that MFSD2A plays a critical role in different tumors. In combination with clinical sample analysis, the prognosis of patients with relatively high expression of MFSD2A in gastric cancer is good, however, no report on diagnosis and treatment of MFSD2A in gastric cancer has been found so far. Therefore, the function of MFSD2A in gastric cancer is revealed to have guiding significance in clinical anti-tumor research.
Disclosure of Invention
In order to solve the defects in the background art, the invention aims to provide the application of MFSD2A serving as a marker in preparing, screening or treating gastric cancer medicaments, and solve the problem of low early diagnosis rate of gastric cancer in the prior art.
The aim of the invention can be achieved by the following technical scheme:
the application of a gastric cancer marker, wherein the marker is an MFSD2A gene or an expression product thereof, comprises the steps of constructing a gastric cancer early screening model, preparing a gastric cancer diagnosis product and preparing a drug for preventing and treating gastric cancer.
Further, the input variable of the model is the abundance of the MFSD2A gene or its expression product.
Further, the products for screening and diagnosing the esophageal cancer comprise reagents, test paper, chips and kits.
Further, the medicament includes an agent that promotes an increase in abundance of the MFSD2A gene expression product.
Further, the agent includes an agent that inhibits prostaglandin secretion.
The application of a gastric cancer marker in preparing a gastric cancer kit is provided, wherein the marker is an MFSD2A gene or an expression product thereof.
A gastric cancer kit, wherein a gastric cancer marker is arranged in the kit, and is MFSD2A gene or an expression product thereof.
Further, the kit comprises a positive control, a negative control, RT-QPCR reaction liquid and MFSD2A gene expression promoter.
The invention has the beneficial effects that:
the invention provides a novel stomach cancer marker, and provides a novel method and a novel target for diagnosis and treatment of stomach cancer.
Drawings
In order to more clearly illustrate the embodiments of the present invention or the technical solutions in the prior art, the drawings used in the description of the embodiments or the prior art will be briefly described, and it will be obvious to those skilled in the art that other drawings can be obtained according to these drawings without inventive effort;
FIG. 1 is a diagram showing the expression of MFSD2A in gastric cancer tissue;
FIG. 2 is a graph showing the expression of MFSD2A in gastric cancer tissues of different stages;
FIG. 3 is a diagram of MFSD2A siRNA interference efficiency characterization;
FIG. 4 is a graph showing the effect of MFSD2A knockout on gastric cancer cell tumorigenicity;
FIG. 5 is a graph showing the effect of MFSD2A knockout on gastric cancer cell invasion;
FIG. 6 is a diagram of MFSD2A overexpression and knock-out efficiency characterization;
FIG. 7 is a graph of the effect of MFSD2A knockout on gastric cancer cell growth in vivo, A: subendothelial tumor size; b: tumor statistics; c: a tumor growth curve;
FIG. 8 is a graph showing the effect of MFSD2A overexpression on gastric cancer cell growth in vivo, A: subendothelial tumor size; b: tumor statistics; c: a tumor growth curve;
FIG. 9 is the effect of MFSD2A knockout on gastric cancer cell immunosuppressive signaling;
FIG. 10 is a graph showing the effect of MFSD2A knockout on gastric cancer cell TGF-beta 1 expression.
FIG. 11 is a graph showing the effect of MFSD2A overexpression or knock-out on gastric cancer cell TGF-beta 1 release;
FIG. 12 is the effect of MFSD2A knockout on the p38 signaling pathway in gastric cancer cells;
FIG. 13 is a graph showing the effect of p38 inhibitors or TGF-beta 1 blockers on gastric cancer cell TGF-beta 1 release;
FIG. 14 is a graph showing the effect of a p38 inhibitor or TGF-beta 1 blocker on the p38 signaling pathway of gastric cancer cells;
FIG. 15 is a graph showing the effect of MFSD2A overexpression on gastric cancer cell prostaglandin metabolism;
FIG. 16 is a graph showing the effect of MFSD2A knockout on gastric cancer cell prostaglandin metabolism;
FIG. 17 is a graph showing the effect of gastric cancer cell prostaglandin anabolism on TGF-beta 1 release,
Detailed Description
The following description of the embodiments of the present invention will be made clearly and completely with reference to the accompanying drawings, in which it is apparent that the embodiments described are only some embodiments of the present invention, but not all embodiments. All other embodiments, which can be made by those skilled in the art based on the embodiments of the invention without making any inventive effort, are intended to be within the scope of the invention.
Example 1: as shown in fig. 1-2, MFSD2A is low expressed in gastric cancer tissue;
experimental materials
Gastric cancer tissue chip is purchased from Shanghai core superliving, MFSD2A primary antibody is purchased from abcam company, and horseradish peroxidase-labeled secondary antibody is purchased from CST company
(II) Experimental methods
Gastric cancer tissue chips were baked overnight at 56 ℃. Dewaxing and hydrating the chip; renaturation of MFSD2A antigen in citrate buffer; slides were incubated with rabbit anti-MFSD 2A (1:600, polyclonal, abcam, maryland, USA) at 37 ℃. After washing with phosphate buffered saline, the secondary antibody was incubated at 37℃for 30min. Finally, the sections were visualized by photographing after Diaminobenzidine (DAB) staining, hematoxylin counterstaining and neutral glue sealing. The immunohistochemical results of MFSD2A were scored by staining intensity (no staining: 0; light yellow: 1; yellow: 2; brown: 3) and positive cell percentages (.ltoreq.10%: 1;11-50%:2;51-75%:3; >75%: 4).
(III) experimental results:
we analyzed the expression of MFSD2A in gastric and paracancestral tissues by immunohistochemical staining. The results show that MFSD2A is expressed lower in gastric cancer tissue than in paracancerous tissue and is associated with gastric cancer stage, the later the stage, the lower the MFSD2A expression.
The above results indicate that MFSD2A is low expressed in gastric cancer tissues.
Example 2: as shown in fig. 3-5, MFSD2A inhibited gastric cancer cell growth and metastasis in vitro;
experimental materials
Plasmid transfection reagent was purchased from Polyplus, QPCR detection reagent and reverse transcription reagent were purchased from Nanjinovirzan, agarose was purchased from Shanghai Biotechnology, soft agar was purchased from Shanghai Michelin, matrigel was purchased from BD biosciences.
(II) Experimental methods
3 MFSD2A specific siRNAs were designed, transferred into MGC803 and AGS cells by INTERREIN transfection reagent, collected after 48 hours, extracted RNA after Trizol cleavage, reverse transcribed into cDNA, and qPCR detected the MFSD2A expression. And simultaneously, extracting proteins by using a SDS (sodium dodecyl sulfate) lysis method after collecting cells, and detecting the expression condition of the MFSD2A by WB.
The MFSD2A specific siRNA gene sequences are respectively as follows:
SEQ ID NO1:5′-AAUAGGUCUGGCCGUGUGGTT-3′；
SEQ ID NO2:5′-UUGAUGUAUGGGCCGUGGCTT-3′；
SEQ ID NO3:5′-AAGCCCAAGGUGUAGGUGCTT-3′；
the interfering RNA gene sequence of the specific siRNA is that,
SEQ ID NO4:5′-UUGAUGUAUGGGCCGUGGCTT-3′。
selecting siRNA with highest interference efficiency for transfection, collecting cells after 48 hours and counting, diluting to 3 x 10 4 cells/mL, 0.1mL of cell suspension was mixed with 1.25mL of ldmem medium and 0.15mL of 4% sterile soft agar, added to a 33mm dish, cultured in a 37 degree incubator for 14 days, photographed under observation under a split microscope and counted.
Cells were digested 48 hours after transfection. Dilution to 5 x 10 with serum-free DMEM resuspension count 5 cells/mL, transwell chamber half an hour in advance, pretreatment with Matrigel diluted 1:7, aspiration of Matrigel, addition of 1X 10 5 5 cells, 600uL of complete culture medium is added into the outer hole of the cell, after culturing for 24 hours at 37 ℃, the membrane is taken down for Rayleigh staining, and photographing statistics are carried out.
(III) results of experiments
qPCR results show that the interference efficiency of three siRNAs exceeds 80%, and WB detection results show that the MFSD2A is obviously inhibited at the protein level, so that the MFSD2A expression is interfered, and the tumorigenicity and invasive capacity of gastric cancer cells can be obviously promoted.
The above results indicate that MFSD2A is capable of inhibiting gastric cancer cell growth and invasion.
Embodiment III: as shown in fig. 6-8, MFSD2A inhibited gastric cancer cell growth in vivo;
experimental materials
Homologous recombinase is purchased from Nanjinopran, DNA endonuclease is purchased from TAKARA, nude mice are purchased from Beijing Vetong Lihua, MFSD2A shRNA lentiviruses are purchased from Shanghai and metaorganisms, and jetPEI transfection reagent is purchased from polyplus;
(II) Experimental methods
The MFSD2A CDS sequence was queried on the NCBI website and cloned into pcdna3.1 vector. And (3) transfecting the MFSD2A over-expression vector or shRNA lentivirus into MGC803 cells to construct an MFSD2A over-expression and MFSD2A knockout stable transgenic cell strain.
MFSD2A knockout stable transgenic strain, MFSD2A overexpression stable transgenic strain and control cells at 2×10 6 Cells/100 μl PBS/mouse back subcutaneous injection, tumor size and body weight of mice were measured every 3 days, experiments were terminated after 3 weeks, mice were euthanized, tumor-stripped photographed, weighed and statistically analyzed.
(III) results of experiments
We first constructed an MFSD2A knockout and overexpressed MGC803 gastric cancer cell line. In vivo experiments show that the low expression of the MFSD2A can promote the growth of gastric cancer in vivo, and the over expression of the MFSD2A can obviously inhibit the growth of gastric cancer cells.
The above results indicate that MFSD2A is capable of inhibiting gastric cancer cell growth in vivo.
Embodiment four: as shown in fig. 9-11, MFSD2A inhibited gastric cancer cell tgfβ1 release
Experimental materials
TGF-beta 1ELISA kit was purchased from Shanghai Daidaceae as
(II) Experimental methods
After 48 hours of transfection of MFSD2A siRNA with MGC803 cells, cells were collected, lysed with 1.5mL Trizol, 500uL of extracted RNA was reverse transcribed into cDNA, the MFSD2A interference efficiency was identified, and the remaining lysed samples were subjected to transcriptome sequencing.
MGC803 cells and AGS cells were transfected with MFSD2A siRNA for 48 hours, and the cells were collected to extract RNA. Reverse transcription to cDNA, the effect on TGF-beta 1mRNA expression following MFSD2A interference was detected by qPCR.
Take 5 x 10 5 MFSD2A overexpressing or knocked out gastric cancer cells and control cells were plated in 6-well plates, cultured for 48 hours, the culture supernatant was aspirated, and tgfβ1 secretion was detected using tgfβ1ELISA kit.
(III) results of experiments
After interference of MFSD2A expression in gastric cancer cell MGC803, transcriptome sequencing is carried out, and gene expression profile analysis shows that MFSD2A low expression promotes TGF beta 1 expression in gastric cancer cells, qPCR detection further verifies the result, ELISA detection results show that MFSD2A over-expression inhibits gastric cancer cells from releasing TGF beta 1, and MFSD2A low expression promotes gastric cancer cells from releasing TGF beta 1.
The above results suggest that MFSD2A is capable of inhibiting the release of veracell tgfβ1.
Fifth embodiment: as shown in fig. 12-14, tgfβ1 autocrine activates the p38 signaling pathway in gastric cancer cells;
experimental materials
p-p38, p38 antibodies were purchased from CST, SB203580 inhibitor from selselect, tgfβ1 blocker distitemide from MCE.
(II) Experimental methods
After 48 hours of transfection of MFSD2A siRNA with MGC803 cells and AGS cells, total protein was extracted from the cells collected and WB was tested for p38 signaling pathway activation.
MGC803 cells were transfected with MFSD2A siRNA for 24 hours, p38 inhibitor or tgfβ1 blocker was added, cell supernatants were aspirated 24 hours later, and tgfβ1 release was detected by ELISA. The cells were harvested to extract total protein and WB was tested for p38 signaling pathway activation.
(III) results of experiments
WB results suggest that MFSD2A low expression activates the gastric cancer intracellular p38 signaling pathway. After MFSD2A is under expressed, the addition of p38 inhibitors or tgfβ1 blockers does not inhibit tgfβ1 release, and both compounds inhibit p38 pathway activation.
The above results demonstrate that MFSD2A underexpression activates the p38 signaling pathway by promoting tgfβ1 release.
Fifth embodiment: as shown in fig. 15-17, MFSD2A inhibited tgfβ1 secretion by restricting prostaglandin synthesis
Experimental materials
Prostaglandin E2, arachidonic acid, COX inhibitors, PLA2 inhibitors were purchased from MCE
(II) Experimental methods
Gastric cancer cells and control cells after MFSD2A overexpression or siRNA interference are collected, lipid metabonomics detection is carried out, and differential components are analyzed.
MFSD2A over-expressed or knocked-out gastric cancer cells were treated with prostaglandin E2, arachidonic acid, COX inhibitor, PLA2 inhibitor, respectively, and ELISA to detect tgfβ1 release levels.
(III) results of experiments
Lipid metabolism detection results show that the MFSD2A over-expression inhibits the synthesis of prostaglandin in gastric cancer cells, the MFSD2A expression is interfered to promote the synthesis of prostaglandin in gastric cancer cells, a prostaglandin compound (PGE 2) and arachidonic acid (ARA) are used for acting on MFSD2A over-expression cell lines, or a COX inhibitor and PLA2 inhibitor are used for acting on MFSD2A knockout cell lines, the release of TGF beta 1 is detected by ELISA, and the fact that both the prostaglandin compound (PGE 2) and the arachidonic acid (ARA) can eliminate the phenomenon of reduced TGF beta 1 release caused by the over-expression of the MFSD2A, and the COX inhibitor and the PLA2 inhibitor of the prostaglandin synthesis rate-limiting enzyme can eliminate the phenomenon of increased TGF beta 1 release caused by the knockout of the MFSD 2A.
The above results indicate that MFSD2A inhibits tgfβ1 release by limiting prostaglandin synthesis.
Further, MFSD2A low expression in the implementation four promotes tgfβ1 expression at the gene level and on average at the protein level. The effect of MFSD2A on TGF-beta 1 production in the present invention is illustrated by transcriptional regulation.
Further, neither the p38 inhibitor nor the tgfβ1 blocker in the fifth implementation inhibit tgfβ1 release, since the tgfβ1 blocker only blocks tgfβ1 binding to the receptor, but not tgfβ1 release.
Further, the tgfβ1 blockers in the examples described above are capable of inhibiting p38 pathway activation, whereas p38 inhibitors are not capable of inhibiting tgfβ1 expression, indicating that MFSD2A modulates p38 pathway activation by inhibiting tgfβ1 release.
The foregoing has shown and described the basic principles, principal features and advantages of the invention. It will be understood by those skilled in the art that the present invention is not limited to the embodiments described above, and that the above embodiments and descriptions are merely illustrative of the principles of the present invention, and various changes and modifications may be made without departing from the spirit and scope of the invention, which is defined in the appended claims.
Claims (10)
1. The application of a gastric cancer marker, wherein the marker is an MFSD2A gene or an expression product thereof, is characterized by comprising the steps of constructing a gastric cancer early screening model, preparing a product for diagnosing gastric cancer and preparing a medicament for preventing and treating gastric cancer.
2. The use of a gastric cancer marker according to claim 1, wherein the input variable of the model is the abundance of the MFSD2A gene or its expression product.
3. The use of a gastric cancer marker according to claim 1, wherein the marker screening and esophageal cancer diagnosis products comprise reagents, test papers, chips and kits.
4. The use of a gastric cancer marker according to claim 1, wherein the medicament comprises an agent that promotes MFSD2A gene expression.
5. The use of a gastric cancer marker according to claim 1, wherein the MFSD2A specific siRNA gene sequences are SEQ ID NO1, SEQ ID NO2 and SEQ ID NO3, respectively.
6. The use of a gastric cancer marker according to claim 4, wherein the agent comprises an agent that inhibits prostaglandin secretion.
7. The application of a gastric cancer marker in preparing a gastric cancer kit is characterized in that the marker is an MFSD2A gene or an expression product thereof.
8. A gastric cancer kit, wherein a gastric cancer marker is arranged in the kit, and is characterized in that the gastric cancer marker is an MFSD2A gene or an expression product thereof.
9. The kit of claim 8, wherein the kit comprises a positive control, a negative control, an RT-QPCR reaction solution, and an MFSD2A gene expression promoter.
The MFSD2A gene is used as a molecular target of gastric cancer and is applied to the preparation of medicines for screening and preventing, relieving and/or treating gastric cancer.
Priority Applications (1)
| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| CN202211147524.4A CN116497117A (en) | 2022-09-19 | 2022-09-19 | Application of MFSD2A as marker in preparation, screening or treatment of gastric cancer drugs |
Applications Claiming Priority (1)
| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| CN202211147524.4A CN116497117A (en) | 2022-09-19 | 2022-09-19 | Application of MFSD2A as marker in preparation, screening or treatment of gastric cancer drugs |
Publications (1)
| Publication Number | Publication Date |
|---|---|
| CN116497117A true CN116497117A (en) | 2023-07-28 |
Family
ID=87318956
Family Applications (1)
| Application Number | Title | Priority Date | Filing Date |
|---|---|---|---|
| CN202211147524.4A Pending CN116497117A (en) | 2022-09-19 | 2022-09-19 | Application of MFSD2A as marker in preparation, screening or treatment of gastric cancer drugs |
Country Status (1)
| Country | Link |
|---|---|
| CN (1) | CN116497117A (en) |
Citations (3)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| US20170037480A1 (en) * | 2014-04-11 | 2017-02-09 | Whitehead Institute For Biomedical Research | Hsf1 in tumor stroma |
| US20210164054A1 (en) * | 2019-12-02 | 2021-06-03 | City Of Hope | Biomarkers for cancer immunotherapy outcomes |
| CN114085868A (en) * | 2020-08-24 | 2022-02-25 | 中国医学科学院肿瘤医院 | Targeting vector, recombinant Huh7 cell line, construction method and application |
-
2022
- 2022-09-19 CN CN202211147524.4A patent/CN116497117A/en active Pending
Patent Citations (3)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| US20170037480A1 (en) * | 2014-04-11 | 2017-02-09 | Whitehead Institute For Biomedical Research | Hsf1 in tumor stroma |
| US20210164054A1 (en) * | 2019-12-02 | 2021-06-03 | City Of Hope | Biomarkers for cancer immunotherapy outcomes |
| CN114085868A (en) * | 2020-08-24 | 2022-02-25 | 中国医学科学院肿瘤医院 | Targeting vector, recombinant Huh7 cell line, construction method and application |
Non-Patent Citations (2)
| Title |
|---|
| XI SH等: "MFSD2A expression predicts better prognosis in gastric cancer", BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, vol. 505, no. 3, pages 699 - 704 * |
| 安松林, 等: "主要促进因子超家族成员MFSD2A对肝癌细胞增殖、凋亡和侵袭的影响", 首都医科大学学报, vol. 42, no. 6, pages 1000 - 1006 * |
Similar Documents
| Publication | Publication Date | Title |
|---|---|---|
| Cao et al. | Enterotoxigenic Bacteroides fragilis promotes intestinal inflammation and malignancy by inhibiting exosome-packaged miR-149-3p | |
| Tu et al. | Over-expression of eukaryotic translation initiation factor 4 gamma 1 correlates with tumor progression and poor prognosis in nasopharyngeal carcinoma | |
| Kang et al. | Energy stress-induced lncRNA HAND2-AS1 represses HIF1α-mediated energy metabolism and inhibits osteosarcoma progression | |
| Peng et al. | Antiproliferative effects by Let-7 repression of high-mobility group A2 in uterine leiomyoma | |
| Zhang et al. | miR34a/GOLPH3 axis abrogates urothelial bladder cancer chemoresistance via reduced cancer stemness | |
| Qi et al. | Targeting the Wnt-regulatory protein CTNNBIP1 by microRNA-214 enhances the stemness and self-renewal of cancer stem-like cells in lung adenocarcinomas | |
| Wang et al. | Relation between the expression of mitotic centromere–associated kinesin and the progression of squamous cell carcinoma of the tongue | |
| CN113476618B (en) | Application of miR-199a-3p in preparation of medicine for treating nasopharyngeal carcinoma | |
| Song et al. | circPTPN12/miR-21–5 p/∆ Np63α pathway contributes to human endometrial fibrosis | |
| CN114686461B (en) | Application of deubiquitinase USP45 in preparation of medicines for treating lung squamous carcinoma | |
| CN114668846B (en) | Application of deubiquitinase USP45 in preparation of medicines for treating esophageal cancer | |
| Li et al. | MicroRNA-144-3p inhibits tumorigenesis of oral squamous cell carcinoma by downregulating ERO1L | |
| Zhou et al. | miR-200b/c-RAP1B axis represses tumorigenesis and malignant progression of papillary thyroid carcinoma through inhibiting the NF-κB/Twist1 pathway | |
| CN113908283A (en) | PRMT5 inhibitor and application thereof in combination with PD-L1 antibody blocking agent in treatment of lung cancer | |
| Nie et al. | Progesterone-induced miR-152 interferes with embryonic implantation by downregulating GLUT3 in endometrial epithelium | |
| Zhang et al. | CircRNA_Maml2 promotes the proliferation and migration of intestinal epithelial cells after severe burns by regulating the miR-93-3p/FZD7/Wnt/β-catenin pathway | |
| CN109468380B (en) | Application of IL1R2 in breast cancer prognosis evaluation and targeted therapy | |
| CN113584173A (en) | Application of lncRNA SLC25A21-AS1 AS esophageal squamous carcinoma marker | |
| CN116808218A (en) | Use of biomarkers in head and neck squamous cell carcinoma treatment | |
| CN116270710A (en) | Application of circRBM33 as target in diagnosis and treatment of prostate cancer | |
| CN113913511B (en) | Application of OTULINs in preparation of reagent for diagnosing and treating cilia-related diseases | |
| CN116497117A (en) | Application of MFSD2A as marker in preparation, screening or treatment of gastric cancer drugs | |
| Shu et al. | BRCA1 Insufficiency Induces a Hypersialylated Acidic Tumor Microenvironment That Promotes Metastasis and Immunotherapy Resistance | |
| CN114592051B (en) | Biomarker and kit for auxiliary diagnosis of myocardial injury | |
| CN115074445B (en) | Application of ENO3 in diagnosis and treatment of kidney cancer |
Legal Events
| Date | Code | Title | Description |
|---|---|---|---|
| PB01 | Publication | ||
| PB01 | Publication | ||
| SE01 | Entry into force of request for substantive examination | ||
| SE01 | Entry into force of request for substantive examination |