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
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- 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
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- gastric cancer
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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.
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