CN111139239B - Application of brand new PANC754 in preparing tumor inhibiting medicine - Google Patents

Application of brand new PANC754 in preparing tumor inhibiting medicine Download PDF

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CN111139239B
CN111139239B CN202010029513.0A CN202010029513A CN111139239B CN 111139239 B CN111139239 B CN 111139239B CN 202010029513 A CN202010029513 A CN 202010029513A CN 111139239 B CN111139239 B CN 111139239B
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CN111139239A (en
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丁伟峰
郭士成
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Affiliated Hospital of Nantong University
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    • C12N15/09—Recombinant DNA-technology
    • C12N15/11—DNA or RNA fragments; Modified forms thereof; Non-coding nucleic acids having a biological activity
    • C12N15/113—Non-coding nucleic acids modulating the expression of genes, e.g. antisense oligonucleotides; Antisense DNA or RNA; Triplex- forming oligonucleotides; Catalytic nucleic acids, e.g. ribozymes; Nucleic acids used in co-suppression or gene silencing
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    • 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
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    • C12Q2600/00—Oligonucleotides characterized by their use
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    • Y02A50/30—Against vector-borne diseases, e.g. mosquito-borne, fly-borne, tick-borne or waterborne diseases whose impact is exacerbated by climate change

Abstract

The invention belongs to the technical field of medicine, and discovers that ENSG00000213754.2 is a brand new tumor inhibition ncRNA through whole genome big data analysis, and the invention names the ENSG00000213754.2 as PANC754(PAn‑cancer Non‑Coding RNA 754, Pan-cancerous non-coding RNA 754); the invention provides an application of a brand new PANC754 in preparing a tumor inhibiting medicament. The embodiment of the invention also provides a brand new verification method for preparing the tumor inhibiting medicine by the PANC754, which comprises the steps that the PANC754 is in a wide low expression mode in 23 cancers; the survival rate of patients with low PANC754 expression in 23 cancers is significantly lower than that of patients with high PANC754 expression; the invention is applied to the discovery of cancer suppressing elements in the universal cancer ncRNA, removes the limitation of the traditional tumor suppressing gene screening, discovers a brand new tumor suppressing ncRNA-PANC 754, and has a wide tumor suppressing effect.

Description

Application of brand new PANC754 in preparing tumor inhibiting medicine
Technical Field
The invention belongs to the technical field of medicines, and relates to the discovery that ENSG00000213754.2 is a brand new tumor inhibition ncRNA through whole genome big data analysis, and can have a wide tumor inhibition effect; the invention names it as PANC 754%PAn-cancer Non-Coding RNA754Pan-cancerous non-coding RNA 754); in particular to an application of a brand new PANC754 in preparing a tumor inhibiting medicament.
Background
In the last decade, although the incidence and mortality of cancer has declined, cancer remains the second leading killer in human health. Cancers, represented by liver cancer, stomach cancer and colorectal cancer, are also the second leading causes of health threats to Chinese. Oncogenes and oncogenes (TSGs) are two major gene types involved in tumorigenesis. Oncogenes result in uncontrolled growth of cells, whereas TSGs generally act as negative regulators of oncogenes, cell cycle checkpoints or gene products, inhibiting the development and progression of cancer. Classical oncogenes are RB (retinoblastoma gene) and TP53 (tumor protein P53). Subsequently discovered oncogenes include ATM (telangiectasia mutated gene), BRCA1 (breast oncogene 1), BRCA2, BRIP1 (BRCA 1 interacting protein carboxy-terminal helicase 1), PALB1 (BRCA 1 partner and locator gene), NF1 (neurofibromatosis type i protein), PMS2 (PMS 1 homolog 2), MSH6 (human MutS homolog 6), BUB1 (spindle checkpoint protein), BUBR1 (BUB 1-related kinase 1), TGF- βrii (transforming growth factor β receptor 2), SMAD4 (parent anti-human drosophila homolog 4), pparγ (peroxisome proliferator-activated receptor γ), P16, PTEN (human chromosome 10 deleted phosphatase and tensin homolog gene), SMARCB1 (SWI/SNF-related matrix-dependent chromatin depends on regulator B family member 1 of actin), and the like.
Non-coding RNAs (ncrnas) are a class of RNA molecules that are not translated into proteins, including transfer RNAs (tRNAs), ribosomal RNAs (rRNAs), microRNAs, siRNAs, piRNAs, snoRNAs, exRNAs, snRNAs, scaRNAs, circRNAs, and lncRNAs. Early studies considered it as "garbage" of the genome, but with increasing evidence that ncRNA genes are deeply involved in the development and progression of disease, it is becoming increasingly important to study their role in disease pathogenesis. In particular, the role and mechanism by which ncRNAs play in tumor suppression will be particularly important. Traditional tumor suppressor gene screening is limited primarily to protein-encoding genes, and expansion of the screening of tumor suppressor elements to include non-protein-encoding genes/regions can allow the discovery of new TSGs.
Traditional tumor suppressor gene screening is mainly limited to protein coding genes, and currently, with development of exon sequencing technology and the like, it is more and more difficult to find new tumor suppressor genes based on coding regions. The RNA in the human genome can be used as an information carrier and can perform a catalytic function, and is considered to be the oldest molecule of life origin. Among them, the non-coding RNA (ncRNA) gene is used as a dark substance of the genome, which accounts for about 98% of the genome, and more researches find that the ncRNA is widely involved in various links of life phenomena, such as growth, differentiation, development and immunity, and has important regulation and control effects even in the formation of tumors.
Disclosure of Invention
The invention aims to provide a novel application of PANC754 in preparing tumor inhibiting medicaments.
In order to solve the technical problems, the embodiment of the invention provides a brand new application of PANC754 in preparing tumor inhibiting medicines.
Further, the tumor inhibiting medicine at least comprises PANC754.
Wherein the PANC754 is ENSG00000213754.2.
Wherein the PANC754 is analyzed by whole genome big data and is analyzed with a pan-cancer analysis as a research tool.
An embodiment of the present invention also provides a completely new PANC754, wherein the PANC754 is an ENSG00000213754.2.
The embodiment of the invention also provides a brand new verification method of the tumor inhibition drug prepared by the PANC754, which is characterized by comprising the following steps:
(1) PANC754 was in a broad low expression pattern in 23 cancers; the low expression of PANC754 was verified in colorectal and gastric cancer patient tissues;
(2) Through meta analysis and Cox regression analysis at the whole genome level, it is verified that patients with low expression of PANC754 have significantly lower survival rates in 23 cancers than those with high expression of PANC754;
(3) Through in vitro experiments, PANC754 gene cDNA is overexpressed in six liver cancer, gastric cancer, esophageal cancer and colorectal cancer cell lines, and PANC754 can obviously inhibit proliferation, clone formation, invasion and metastasis of tumor cells;
(4) According to the characteristic that PANC754 is antisense ncRNA, based on the sequence complementation principle of the antisense ncRNA, through whole genome blast analysis, the PANC754 sequence similarity genes are KPNA4 and MTMR8, and through immunoblotting experiments, it is verified that PANC754 can interact with target genes KPNA4 and MTMR 8;
(5) Bioinformatics excavates the expression correlation of PANC754 expression and whole genome gene, and then through fluorescent quantitative PCR experiments, it is verified that PANC754 can directly regulate CDK2, DNMT1 and NRAS gene mRNA expression through a co-expression form, wherein CDK2 has direct correlation, R= -0.05, P=4.9x10 -9 It is suggested that the inhibition of cancer can be achieved through the KPNA4-CDK2 signaling pathway.
The technical scheme of the invention has the following beneficial effects: the invention focuses on a novel cancer suppressing element, namely non-coding RNA, so as to find a novel cancer treatment target; the invention is applied to the discovery of cancer suppressing elements in the universal cancer ncRNA, removes the limitation of the traditional tumor suppressing gene screening, and further discovers a brand new tumor suppressing ncRNA-PANC 754, wherein the PANC754 has a wide tumor suppressing effect.
Drawings
FIG. 1 is a schematic diagram of a medium genome-wide RNA analysis screening PANC754 and verifying its low expression profile in an embodiment of the present invention;
FIG. 2 is a graph showing the verification of the low expression pattern of PANC754 in 23 cancers found by Meta analysis in the examples of the present invention;
FIG. 3 is a graph showing the overall survival of the meta analysis and Cox regression analysis PANC754 at the whole genome level in the examples of the present invention;
FIG. 4 is a diagram showing that PANC754 significantly inhibits tumor cell proliferation and clonogenesis in examples of the present invention;
fig. 5 is a verification graph of the palc 754 significantly inhibiting tumor cell invasion and metastasis in an embodiment of the present invention;
FIG. 6 is a diagram showing the verification of the discovery of a typical PANC754 sequence similarity gene by whole genome blast analysis in an embodiment of the invention;
FIG. 7 is a verification graph of immunoblotting experiments to find that PANC754 can interact with target genes KPNA4 and MTMR8 in the embodiment of the present invention;
FIG. 8 is a graph showing the verification of the expression of COPS7B, PMVK, SMIM, CDK2, DNMT1 and SRSF genes by PANC754 regulation by fluorescence quantitative PCR experiment in the embodiment of the invention.
Detailed Description
In order to make the technical problems, technical solutions and advantages to be solved more apparent, the following detailed description will be given with reference to the accompanying drawings and specific embodiments.
Through whole genome big data analysis, ENSG00000213754.2 is found to be a brand new tumor inhibition ncRNA, and can have a wide tumor inhibition effect. The invention names it as PANC 754%PAn-cancer Non-Coding RNA754Non-coding RNA 754) of pan-carcinoma and related application protection.
An application of PANC754 in preparing tumor inhibiting medicines.
In a further embodiment, the tumor suppressor drug comprises at least PANC754. Wherein the PANC754 is ENSG00000213754.2. Wherein the PANC754 is analyzed by whole genome big data and is analyzed with a pan-cancer analysis as a research tool.
Embodiments of the present invention also provide a totally new PANC754, the PANC754 being an ENSG00000213754.2.
The embodiment of the invention also provides a brand new verification method of the tumor inhibiting medicine prepared by the PANC754, which comprises the following steps:
(1) PANC754 showed a broad low expression pattern in 23 cancers (whole genome screen results are shown in fig. 1A and 2); the low expression of PANC754 was verified in colorectal and gastric cancer patient tissues (clinical sample verification results are shown in fig. 1B and 1C). FIG. 1A, manhattan, shows that the TCGA database was screened for genomic RNA sequencing data from 23 cancers to generate PANC754; fig. 1b, quantitative PCR results for 30 colorectal cancer tissues and 26 paracancerous control tissues show that PANC754 is expressed low in the straightened cancer tissues (p=0.0269) relative to the paracancerous control tissues; FIG. 1C shows that PANC754 was expressed less in gastric cancer tissue (P<0.001). FIG. 2, forest map of regression analysis of 10490 gene expression data in 23 cancers combined with fixed effect model (fixed effect model) and random effect model (random effect model) shows that PANC754 is ubiquitously expressed in cancer tissue (SMD= -1.2), where the fixed effect model P<1.0x10 -264 The method comprises the steps of carrying out a first treatment on the surface of the Random effect model p=1.78x10 -29 。
(2) Patients with low PANC754 expression were found to have significantly lower survival rates in 23 cancers than those with high PANC754 expression by metaanalysis at the whole genome level and Cox regression analysis, and the results are shown in fig. 3, where palc 754 was cancer by a forest map of regression analysis of 8074 survival rate data in 23 cancers, combined with a fixed effect model (fixed effect model) and a random effect model (random effect model)A protective factor wherein the fixed effect model risk factor hr=0.84, 95% ci:0.76-0.94, p=0.0024; random effect model hr=0.86, 95% ci:0.78-0.94, p=9.0x10 -4 。
(3) Through in vitro experiments, the PANC754 gene cDNA is overexpressed in six liver cancer, gastric cancer, esophageal cancer and colorectal cancer cell lines, and the PANC754 can remarkably inhibit proliferation, clone formation, invasion and metastasis of tumor cells (verification results are shown in fig. 4 and 5). Fig. 4a, cck8 experiments found that PANC754 was overexpressed in gastric cancer cell line MGC803, with significantly lower cell proliferation rates than in empty and untransfected plasmid groups (P < 0.001); FIG. 4B, CCK8 experiments found that the cell proliferation rate of PANC754 overexpressed in esophageal cancer cell line Eca109 was significantly lower than in empty and untransfected plasmid groups (P < 0.001); fig. 4C, flow cytometry assays found that the apoptosis rate was significantly increased in the colorectal cancer cell line over-expressing PANC754 group relative to empty and untransfected pellet groups (p=0.0012). FIG. 5A shows that the cell migration capacity of the PANC754 group overexpressed in the liver cancer cell line HepG2 is significantly lower than that of the empty plasmid group and the untransfected plasmid group; fig. 5B, statistical histograms show cell scratch experiments of hepatoma cell lines, over-expressing PANC754 group VS empty plasmid group and untransfected plasmid group (P < 0.001); FIG. 5C shows that the liver cancer cell line Bel-7402 overexpresses PANC754 group and has significantly lower cell invasion capacity than empty plasmid group and untransfected plasmid group; fig. 5D, statistical histograms show cell invasion experiments of liver cancer cell lines, over-expressing PANC754 group VS empty plasmid group and untransfected plasmid group (p=0.0003).
(4) According to the characteristic that PANC754 is antisense ncRNA, based on the sequence complementation principle of the antisense ncRNA, the sequence similarity genes of PANC754 are KPNA4 and MTMR8 as shown in figure 6 through whole genome blast analysis; through immunoblotting experiments, it was verified that PANC754 can interact with its target genes KPNA4 and MTMR8, as shown in fig. 7. Wherein, fig. 6A, using NCBI blastn suite tool, sequence alignment analysis was performed on the PANC754 and 55270388 non-redundant sequences from GenBank, EMBL, DDBJ, PDB and RefSeq databases using default algorithm parameters, and the PANC754 was found to be very highly homologous to KPNA4, MTMR8 gene sequences (score > 1200); FIG. 6B is an evolutionary tree diagram showing that PANC754 has extremely high homology with KPNA4 and MTMR8 gene sequences; FIG. 6C shows that the regulatory targets of the antisense ncRNA PANC754 are KPNA4 and MTMR8 genes based on the sequence complementation theory and by using a heat map of the coexpression analysis. FIG. 7A shows that, compared with empty plasmid groups and untransfected plasmid groups, liver cancer cell line Bel-7402 overexpresses PANC754 groups, and KPNA4 and MTMR8 protein levels are significantly reduced; FIG. 7B, immunoblotting experiments revealed that colorectal cancer cell line DLD1 overexpresses PANC754, with significantly reduced KPNA4 and MTMR8 protein levels relative to empty and untransfected plasmid groups; FIG. 7C, immunoblotting experiments show that the esophageal cancer cell strain Eca109 overexpresses PANC754, and the KPNA4 and MTMR8 protein levels are significantly reduced relative to empty and untransfected plasmid groups; FIG. 7D, immunoblotting experiments show that compared with empty plasmid groups and untransfected plasmid groups, liver cancer cell line HepG2 over-expresses PANC754 groups, and KPNA4 and MTMR8 protein levels are obviously reduced; fig. 7E, immunoblotting experiments found that gastric cancer cell line MGC803 overexpressed PANC754 group with significantly reduced KPNA4 and MTMR8 protein levels relative to empty plasmid group and untransfected plasmid group; FIG. 7F, immunoblotting experiments revealed that colorectal cancer cell line SW480 overexpressed PANC754, with slightly lower KPNA4 and MTMR8 protein levels, relative to empty and untransfected plasmid groups; fig. 7G, statistical histograms show that six cell lines overexpress PANC754 group with significantly reduced KPNA4 protein levels (P < 0.05) relative to empty and untransfected pellet groups; fig. 7H, statistical histograms show that six cell lines overexpress PANC754 group with significantly reduced MTMR8 protein levels (P < 0.05) relative to empty and untransfected plasmid groups.
(5) Bioinformatics excavates the relativity of the expression of the PANC754 and the expression of the whole genome genes, and then through a fluorescent quantitative PCR experiment, the PANC754 is verified to directly regulate the mRNA expression of CDK2, DNMT1 and NRAS genes in a co-expression mode, as shown in figure 8, the fluorescent quantitative PCR experiment discovers that the PANC754 regulates the expression of COPS7B, PMVK, SMIM, CDK2, DNMT1 and SRSF genes; wherein CDK2 has a direct correlation, r= -0.05, p=4.9×10 -9 Prompt available KPNThe A4-CDK2 signaling pathway plays a role in inhibiting cancer. FIG. 8A, based on the sequence similarity analysis of FIG. 6C, selects one of the genes with the most significant co-expression similarity P value, COPS7B, and quantitative PCR detection shows that the COPS7B mRNA level is significantly reduced in the esophageal, gastric, hepatic, colorectal cancer cell lines relative to the empty and untransfected plasmid groups (P<0.05 A) is provided; FIG. 8B, based on the sequence similarity analysis of FIG. 6C, selects one of the genes with the most significant co-expression similarity P value, and quantitative PCR detection shows that the mRNA level of PMVK is significantly reduced (P<0.05 A) is provided; FIG. 8A, based on the sequence similarity analysis of FIG. 6C, selecting one of the most significant genes for co-expression similarity P, quantitative PCR detection revealed that SMIM12 mRNA levels were significantly reduced relative to the empty and untransfected plasmid groups, the esophageal, gastric, liver, colorectal cancer cell lines overexpressing PANC754 group (P<0.05 A) is provided; FIG. 8D, selection of CDK2, one of the most significant oncogenes with regard to P-value co-expression, quantitative PCR detection revealed a significant decrease in CDK2 mRNA levels relative to the empty and untransfected plasmid groups, in the esophageal, gastric, liver and colorectal cancer cell lines (P<0.05 A) is provided; FIG. 8E, DNMT1, one of the oncogenes with the most pronounced P-value of the co-expression correlation, was selected and quantitative PCR detection revealed that DNMT1 mRNA levels were significantly reduced relative to the empty and untransfected plasmid groups, as compared to the PANC754 group overexpressed in esophageal, gastric, liver and colorectal cancer cell lines (P<0.05 A) is provided; FIG. 8F, selection of one of the most significant oncogenes with regard to P-value co-expression, quantitative PCR detection revealed that SRSF2 mRNA levels were significantly reduced relative to the empty and untransfected plasmid groups in the esophageal, gastric, liver, colorectal cancer cell lines over-expressing PANC754 group (P<0.05)。
While the foregoing is directed to the preferred embodiments of the present invention, it will be appreciated by those skilled in the art that various modifications and adaptations can be made without departing from the principles of the present invention, and such modifications and adaptations are intended to be comprehended within the scope of the present invention.
Sequence listing
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<120> application of novel PANC754 in preparing tumor inhibiting medicine
<141> 2020-01-13
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<213> Non-Coding RNA754 for Pan-cancer (PAN-cancer Non-Coding RNA754, PANC 754)
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aacatctctt aaagagaagg aacgtactga atgaagatac ctgtgaagac tgatacaaat 180
gatgattatg gagtgtaaaa tacctctcta gtagctatta ttcaaaatgc ttcaagtgat 240
aactaagaaa ttcaattaaa tgcagttcgg gctgctagga agctttgtcc agtgatcgaa 300
gtctaccaat ttataaaaat aaaatctgga atactacctg ttctagtcta ttgtcttgaa 360
agagatgaca atgctttaca gttagaagct gcatgggctt tgacaaacac tgcatctaga 420
acctctgaac aagctcaaac agtagttcag tccaatgctg tgccacattt cctgaggctc 480
ctccattcac ttcatcagaa tgtttgtgag caagcagtgt gggcattgag aactatcata 540
agtgatggtc ctcccgatgt agagattatg tcataagtct tggagttgtg aaacctttat 600
tttacttcaa aagtgctagc attccaagtg tgagccacca tgcccagcct gggttatggc 660
caatttatgt caccacaaag agccaccacc accaatggaa accatacagg aaatgctttc 720
agctctttgt gttctaattc atcatacatt tgtaaatata ttagtagata cagactgggc 780
cctctcttac cttactggtg ctggcaatga acaaatacag atggtagtag actctggaat 840
agttcctcat ttggttcctc ttctcagccg ccgggtggtt cagactgctg cacctcaagc 900
tgtgagcaac atggctactg gaattgaaga gcaaacagaa gtagttgtga attatgatgc 960
tctttcatac ttgtgggcaa tcctgacaca tcccaaagag aaaattaata aagaggcagt 1020
atggtttctc tgtaacatca ctgcaggtaa tcagctgcag atacaggcag taatagatgc 1080
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ggtggaacat ttggtttcaa tttatctgcc agtataccaa tagaacagtt ccagtt 1436

Claims (3)

1. The application of PANC754 in preparing medicines for inhibiting tumors, wherein the tumors are liver cancer, gastric cancer, esophageal cancer and colorectal cancer, the PANC754 is ENSG00000213754.2, and the sequence of the PANC754 is shown as seq-1.
2. The use of PANC754 for the manufacture of a medicament for the inhibition of tumors according to claim 1, wherein the medicament for the inhibition of tumors comprises at least PANC754.
3. The use of PANC754 for the preparation of a tumor-inhibiting medicament according to claim 1 or 2, wherein the PANC754 is analyzed by whole genome big data analysis and is analyzed by pan-cancer analysis as a research tool.
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US7166573B1 (en) * 1999-05-28 2007-01-23 Ludwig Institute For Cancer Research Breast, gastric and prostate cancer associated antigens and uses therefor

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US7166573B1 (en) * 1999-05-28 2007-01-23 Ludwig Institute For Cancer Research Breast, gastric and prostate cancer associated antigens and uses therefor

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