CN112760321B - Non-coding RNA for inhibiting flood cancer and detection method for flood cancer inhibition attribute of non-coding RNA - Google Patents
Non-coding RNA for inhibiting flood cancer and detection method for flood cancer inhibition attribute of non-coding RNA Download PDFInfo
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Abstract
The invention provides Non-Coding RNA for inhibiting the flood cancer, which is PAn-cancer Non-Coding RNA 246 and is named PANC246. Also provided is a method for detecting the pan-cancer inhibitory property of non-coding RNA for pan-cancer inhibition, comprising the following steps: 2.1, constructing plasmids and culturing a tumor cell line; 2.2, CCK-8 experiments to detect proliferation capacity of tumor cell lines over-expressing PANC 246; 2.3, detecting the apoptosis rate of PANC246 cancer cells by flow cytometry; 2.4, scratch experiments detect the ability of PANC246 to inhibit tumor cell migration; 2.5, transwell laboratory experiments to detect the ability of PANC246 to inhibit tumor cell invasion; 2.6, up-regulating expression of PANC246 to inhibit the mRNA level of protooncogene by fluorescent quantitative PCR detection. The invention discovers a brand new PAn cancer inhibition ncRNA (PANC 246) (PAn-cancer Non-Coding RNA 246) through the PAn cancer data mining in the TCGA database. The patent is used for defining the pan-cancer inhibition property of PANC246 through bioinformatics and functional research so as to provide a new non-coding gene target spot for the treatment of tumors.
Description
Technical Field
The invention belongs to the field of medical and health, and particularly relates to non-coding RNA for inhibiting cancer and a detection method for inhibiting cancer by using the same.
Background
Non-coding RNAs (ncrnas) are a class of RNA molecules that are not translated into proteins, including transfer RNAs (tRNAs), ribosomal RNAs (rRNAs), micro RNA (microRNAs), small interfering RNAs (siRNAs), piwi protein-interacting RNAs (siRNAs), nucleolar RNAs (snoRNAs), extracellular RNAs (exRNAs), small nucleolar RNAs (snRNAs), small cajal body-associated RNAs (small cajal body associated RNAs, scaRNAs), circular RNAs (circRNAs), long-chain non-coding RNAs (lncrrnas), and the like. Early studies considered that ncRNAs were "garbage" of the genome, but more and more evidence suggests that the ncRNA gene is deeply involved in the occurrence and development of diseases, so that research on the role of ncRNAs in disease pathogenesis is important, and research on ncRNAs with cancer-suppressing effect and the mechanism thereof is particularly needed.
Oncogenes and oncogenes (TSGs) are two major gene types involved in the development of 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. Traditional tumor suppressor gene screening is mainly limited to genes encoding proteins, and expansion of the screening to non-protein encoding genes or regions can discover new TSG to discover new pan-cancer suppressing ncRNA in hope of providing new non-encoding gene targets for tumor treatment.
Disclosure of Invention
The technical problem to be solved by the invention is to provide the non-coding RNA for inhibiting the pan-cancer and the detection method of the pan-cancer inhibition attribute thereof, and the pan-cancer inhibition attribute of PANC246 is defined through bioinformatics and functional research so as to provide a new non-coding gene target spot for the treatment of tumors.
In order to solve the above technical problems, an embodiment of the present invention provides a Non-Coding RNA for inhibiting PAn-cancer, which is PAN-cancer Non-Coding RNA 246, and is named PANC246.
The recognition steps of the PANC246 are as follows:
1.1, collecting transcriptome sequencing data of all tumors in a TCGA database;
1.2, extracting 11,529 non-coding RNAs from 11,093 RNA-seq data and performing whole genome meta analysis to identify new pan-cancer regulatory ncrnas;
1.3 by using a random effect model, 1615 ncrnas were found to be significantly up-or down-regulated, with PAn-cancer Non-Coding RNA 246 being the novel ncRNA encoded by ENSG00000231246, PANC246 being significantly down-regulated in 23 human cancer tissues.
The invention also provides a method for detecting the pan-cancer inhibition attribute of the non-coding RNA for pan-cancer inhibition, which comprises the following steps:
2.1, constructing plasmids and culturing a tumor cell line;
2.2, CCK-8 experiments to detect proliferation capacity of tumor cell lines over-expressing PANC 246;
2.3, detecting the apoptosis rate of PANC246 cancer cells by flow cytometry;
2.4, scratch experiments detect the ability of PANC246 to inhibit tumor cell migration;
2.5, transwell laboratory experiments to detect the ability of PANC246 to inhibit tumor cell invasion;
2.6, up-regulating expression of PANC246 to inhibit the mRNA level of protooncogene by fluorescent quantitative PCR detection.
The specific steps of the step 2.1 are as follows:
2.1.1 six cell lines including esophageal cancer cell line Eca109, liver cancer cell lines HepG2 and Bel7402, gastric cancer cell line MGC803, colorectal cancer cell lines SW480 and DLD1, and plasmid pcDNA3.1 were placed in DMEM medium (Kaiyi, nanjin) containing 10% fetal bovine serum (Excell Co., USA) at 37℃and 5% CO 2 An incubator;
2.1.2, chorus ENSG00000231246.1 was synthesized by Kingshi Biotechnology Co., ltd (Nanjing, china) and cloned into pcDNA3.1 plasmid, passed through Lipofectamine3000 (Invitrogen, USA) and then transfected into the above cancer cell line.
The specific steps of the step 2.2 are as follows: 2x10 5 Cells were cultured in 24-well plates, transfected with pcDNA3.1 empty plasmid and PANC246 overexpressing plasmid, and cells were collected at 0, 24, 48, and 72 hours, respectively, and the proliferation capacity of tumor cell lines overexpressing PANC246 was examined by CCK-8 experiments.
The specific steps of the step 2.4 are as follows:
2.4.1, when the cells are 70-80% fused after 24 hours of cell culture, inoculating the cells into a 6-hole culture plate;
2.4.2 gently and slowly scratching the cell layer with a 200. Mu.L pipette tip, gently rinsing 2 times with a medium after scratching to remove the detached cells, and measuring the gap distance as that at 0 h;
2.4.3, to determine the cell migration ability, the gap distance was measured 24h and 48h after the scratch, and the calculation formula of the migration distance was:
distance of migration = gap distance at 0 h-gap distance at t;
wherein t is 24h or 48h.
The specific steps of the step 2.5 are as follows:
2.5.1, pcDNA3.1-PANC246 to be transfected, untransfected control and fine pcDNA3.1Cell suspension (0.5X10) 5 Individual cells/mL) was added to the Transwell chamber while 200 μl of serum-free medium was added, and 500 μl of medium containing 10% fetal bovine serum was added to the lower chamber as a stimulus for invasion transfer;
2.5.2, placing the Transwell cell in a cell incubator for incubation for 24 hours, then performing crystal violet staining on invasive cells on the lower surface of the cell membrane for 10 minutes, photographing under a 40-fold high-power visual field of a microscope, and detecting the invasion capacity of PANC246 to inhibit tumor cells.
The specific steps of the step 2.3 are as follows:
2.3.1 cells were trypsinized and washed twice with pre-chilled Phosphate Buffer (PBS). Add 500. Mu.L of binding buffer (KeyGen) and resuspend to give a 5X 10 cell number 5 A cell;
2.3.2 adding 5. Mu.L of Annexin V-FITC (KeyGen) to the cell suspension and counterstaining the cell suspension with 5. Mu.L of Propidium Iodide (PI);
2.3.2 the mixture was incubated for 10min in the dark at room temperature and then subjected to apoptosis analysis using a FlowSight flow cytometer (Merck, germany).
The specific steps of the step 2.6 are as follows:
2.6.1 Total RNA was collected using TRIzol (Invitrogen, USA) and converted to cDNA using the first strand cDNA Synthesis kit (Vazyme Biotech, china) according to the instructions;
2.6.2 real-time fluorescent quantitative PCR was performed on an ABI 7500PCR apparatus (ABI, USA) using SYBR Green Master Mix (Vazyme Biotech) to detect the inhibition of proto-oncogene mRNA levels by up-regulated expression PANC246.
The technical scheme of the invention has the following beneficial effects: the invention discovers a brand new PAn cancer inhibition ncRNA (PANC 246) (PAn-cancer Non-Coding RNA 246) through the PAn cancer data mining in the TCGA database. The patent is used for defining the pan-cancer inhibition property of PANC246 through bioinformatics and functional research so as to provide a new non-coding gene target spot for the treatment of tumors.
Drawings
FIG. 1 is a graph showing the results of analysis of non-coding RNA for identifying abnormal expression by whole genome in the present invention;
FIG. 2 is a schematic representation of the broad down-regulated expression of PANC246 in 23 human cancers according to the present invention;
FIG. 3 is a graph showing the results of the CCK-8 experiment for detecting proliferation capacity of a tumor cell line over-expressing PANC 246;
FIG. 4 is a graph showing the results of flow cytometry detection of PANC246 pro-cancer apoptosis in the present invention;
FIG. 5 is a graph showing the results of the scratch test of the present invention for the ability of PANC246 to inhibit tumor cell migration;
FIG. 6 is a graph showing the results of a Transwell laboratory test for the ability of PANC246 to inhibit tumor cell invasion in accordance with the present invention;
FIG. 7 is a graph showing the results of up-regulating the mRNA level of the expressed PANC246 gene in the fluorescent quantitative PCR detection of the present invention;
FIG. 8 is a graph showing the results of detecting apoptosis of PANC246 in cancer cells by flow cytometry in accordance with one embodiment of the present invention;
FIG. 9 is a statistical histogram of the scratch test performed in example one to detect that PANC246 inhibits migration of colorectal cancer cells DLD 1;
fig. 10 is a statistical histogram of scratch test detection PANC246 inhibiting migration of esophageal cancer cells Eca109 in example one;
fig. 11 is a statistical histogram of scratch test detection PANC246 inhibiting migration of liver cancer cells HepG2 in example one;
fig. 12 is a statistical histogram of scratch test detection PANC246 inhibiting migration of gastric cancer cells MGC803 in example one;
fig. 13 is a statistical histogram of scratch test detection PANC246 inhibiting migration of colorectal cancer cells SW480 in example one;
fig. 14 is a graph showing the results of the Transwell laboratory test for the ability of PANC246 to inhibit tumor cell invasion in example one.
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.
The invention provides Non-Coding RNA for inhibiting the flood cancer, which is PAn-cancer Non-Coding RNA 246 and is named PANC246.
The recognition step of the PANC246 is:
1.1, collecting transcriptome sequencing (RNA-seq) data of all tumors in the TCGA database;
1.2, extracting 11,529 non-coding RNAs from 11,093 RNA-seq data and performing whole genome meta analysis to identify new pan-cancer regulatory ncrnas;
1.3 by using a random effect model, 1615 ncrnas were found to be significantly up-or down-regulated (fig. 1, bonferroni corrected P<0.05 (v) wherein PAn-cancer Non-Coding RNA 246 (PANC 246) is a novel ncRNA encoded by ENSG00000231246, PANC246 is significantly down-regulated in 23 human cancer tissues (smd= -4.4, P in fixed effect model)<1.0x10 -227 P=3.28x10 in random effect model -21 Fig. 2).
FIG. 1 is a graph of non-coding RNA (ncRNA) results from whole genome analysis to identify aberrant expression, and Manhattan plot (Manhattan plot) shows the ncRNA differentially expressed from pan-cancerous RNA-seq in TCGA dataset found by whole genome meta analysis. Random effect model P values showed significant differences in expression of 1615 ncRNA genes in cancer and paracancerous control tissues.
Fig. 2 is a schematic representation of PANC246 widely down-regulated expression in 23 human cancers, with cancer sample data from the TCGA project (n= 10,490). Prior to meta analysis, the gene expression levels were log2 transformed. And then adopting a fixed effect model and a random effect model for analysis. 95% CI is used to represent the mean and 95% interval of expression. To show more detail of the different studies, any normalized mean difference (SMD) above-15 and below 5 is indicated by arrows. The purple filled rectangle represents the SMD of the fixed effect model and the random effect model.
The invention also provides a method for detecting the pan-cancer inhibition attribute of the non-coding RNA for pan-cancer inhibition, which comprises the following steps:
2.1, constructing plasmids and culturing a tumor cell line;
2.2, CCK-8 experiments to detect proliferation capacity of tumor cell lines over-expressing PANC 246;
to investigate the functional role of PANC246 in cancer cell phenotype, the PANC246 plasmid was transfected in tumor cell lines and the effect of PANC246 overexpression on tumor cell proliferation was analyzed by CCK-8 method. The growth curves of PANC246 transfected gastric cancer cell lines MGC803 and esophageal cancer Eca109 cells were significantly slowed, and proliferation capacity was significantly inhibited, particularly after 48h and 72h (p=0.0004, p=0.0002; fig. 3E and 3C), compared to the control group or pcdna3.1 group. Similar proliferation patterns were also observed for the two hepatoma cell lines HepG2 and Bel-7402 (p=0.00002, p=0.00004; fig. 3D and 3A) and for the two CRC cell lines SW480 and DLD1 (p= 0.00023 and p=0.0007) (fig. 3F and 3B).
FIG. 3 is a graph showing the results of CCK-8 experiments to detect the proliferation potency of tumor cell lines overexpressing PANC246, and FIG. 3A and FIG. 3D liver cancer cell lines overexpress the proliferation potency of PANC 246; fig. 3B and 3F colorectal cancer cell lines overexpress the proliferative capacity of PANC 246; FIG. 3C shows the proliferative capacity of an esophageal cancer cell line over-expressing PANC 246; FIG. 3E gastric cancer cell line overexpresses the proliferative capacity of PANC 246; * P <0.001; * P <0.0001; control: untransfected control group; pcDNA3.1: empty plasmid transfection sets; PANC246: pcDNA3.1-PANC246 plasmid transfection group.
2.3, detecting the apoptosis rate of PANC246 cancer cells by flow cytometry;
to determine whether overexpression of PANC246 could induce increased apoptosis in tumor cells, flow cytometry was used to examine the rate of apoptosis in tumor cells. As shown in fig. 4, the apoptosis rate of CRC cell line SW480 was significantly increased (p=0.0022) after PANC246 transfection compared to the control and pcdna3.1 groups. The same trend of increased apoptosis was also detected in Eca109 (p=0.001), hepG2 (p=0.0045), bel-7402 (p=0.0018), MGC803 (P < 1.0x10-4) and DLD1 (p=5.0x10-4) cell lines.
FIG. 4 is a graph showing the results of flow cytometry detection of PANC246 pro-cancer apoptosis, annexin V-FITC staining for early apoptosis, PI staining for late apoptosis; control: untransfected control group; pcDNA3.1: empty plasmid transfection sets; PANC246: pcDNA3.1-PANC246 plasmid transfection group.
2.4, scratch experiments detect the ability of PANC246 to inhibit tumor cell migration;
through scratch test experiments, as shown in fig. 5A and 5B, the migration distance after 24 hours and 48 hours of the bell 7402 liver cancer cell culture of the pcdna3.1-PANC246 group (abbreviated as PANC 246) was significantly shorter than that of the control group and the pcdna3.1 group, P <0.001 and P <1.0x10-4. Similar results were also observed in Eca109, hepG2, MGC803, SW480 and DLD1 cells at 48h of culture (fig. 5C).
Fig. 5 is a graph showing the result of scratch test for detecting the ability of PANC246 to inhibit tumor cell migration, and fig. 5A shows that the scratch test for PANC246 inhibits migration of hepatoma cell Bel 7402; FIG. 5B is a statistical histogram of scratch assay detection PANC246 inhibiting the migration of hepatoma cell Bel 7402; FIG. 5C statistical histograms of the scratch assay detection PANC246 inhibiting migration of colorectal cancer cells DLD 1; * P <0.001; * P <0.0001; control: untransfected control group; pcDNA3.1: empty plasmid transfection sets; PANC246: pcDNA3.1-PANC246 plasmid transfection group.
2.5, transwell laboratory experiments to detect the ability of PANC246 to inhibit tumor cell invasion;
the effect of over-expression PANC246 on tumor cell invasion was examined by Transwell experiments. It was found that after 48h of culture of Bel7402 hepatoma cells, the PANC246 group had significantly reduced cells invading the Transwell cell membrane compared to the control group and pcdna3.1 group (p=0.0003, fig. 6A and 6B). Meanwhile, studies also found that the invasiveness of Eca109 (p=1.87x10-5), hepG2 (p=0.0004), MGC803 (p=0.0002), SW480 (p=0.0011) and DLD1 (p=0.0007) cells was significantly reduced (fig. 6B).
Fig. 6 is a graph showing the results of a Transwell laboratory test for the ability of PANC246 to inhibit tumor cell invasion, and fig. 6A shows that PANC246 significantly inhibits tumor cell invasion through Transwell cell membrane staining; FIG. 6 statistical histogram of BTranswell laboratory experiments; * P <0.001; * P <0.0001; control: untransfected control group; pcDNA3.1: empty plasmid transfection sets; PANC246: pcDNA3.1-PANC246 plasmid transfection group.
2.6, detecting the condition that the up-regulated expression PANC246 inhibits the mRNA level of the protooncogene by fluorescence quantitative PCR;
some protooncogenes, such as cyclin-dependent kinase 2 (CDK 2), murine sarcoma virus oncogene (KRAS, P21), myoglobin (TTN), mucin 16 (MUC 16, CA 125), phosphatidylinositol-4, 5-bisphosphate kinase catalytic subunit α (PIK 3 CA) and CUB and sechi multiregion complement regulatory protein 3 (CSMD 3) are significantly highly expressed in tumors and promote tumorigenesis development. It is assumed that PANC246, which is a cancer suppressing ncRNA, may suppress the expression of these protooncogenes. As shown in fig. 7, the overexpressed PANC246 significantly inhibited the expression levels of CDK2 gene, KRAS gene, TTN gene, MUC16 gene, PIK3CA gene, and CSMD3 gene mRNA compared to the control and pcdna3.1 groups. It is shown that PANC246 can directly or indirectly regulate and control protooncogene expression to exert cancer suppressing effect.
FIG. 7 is a graph showing the results of fluorescence quantitative PCR detection of up-regulated expression of PANC246 to inhibit the level of protooncogene mRNA, the protooncogene CDK2 of FIG. 7A; FIG. 7B protooncogene CSMD3; FIG. 7C protooncogene KRAS; FIG. 7D proto-oncogene MUC16; FIG. 7E protooncogene PIK3CA; FIG. 7F protooncogene TTN; * P <0.001; * P <0.0001; control: untransfected control group; pcDNA3.1: empty plasmid transfection sets; PANC246: pcDNA3.1-PANC246 plasmid transfection group.
The technical scheme of the invention is further described below in conjunction with specific embodiments.
A detection method for the anti-cancer property of non-coding RNA for anti-cancer specifically comprises the following steps:
I. cell lines and plasmids
Esophageal cancer cell strain Eca109, liver cancer cell strains HepG2 and Bel7402, gastric cancer cell strain MGC803, colorectal cancer cell strains SW480 and DLD1 and plasmid pcDNA3.1 are all stored in the laboratory. Six cell lines were placed in DMEM medium (Kaiyi, nanjing) containing 10% fetal bovine serum (Excell Co., USA) at 37℃with 5% CO 2 An incubator. Full length ENSG00000231246.1 was synthesized by gold strei biotechnology limited (south kyo, china) and cloned into pcdna3.1 plasmid and transfected into the cancer cell line by Lipofectamine3000 (Invitrogen, usa).
II. Cell proliferation assay
2x10 5 Cells were cultured in 24-well plates, transfected with pcDNA3.1 empty plasmid, PANC246 over-expression plasmid, and cells were collected at 0, 24, 48, 72h, respectively,the CCK-8 method was used to calculate the cell proliferation capacity.
III, cell scratch test to detect cell migration Capacity
After 24h of cell culture, cells were at 70-80% confluence and inoculated into 6-well plates. The cell layer was gently and slowly scraped with a 200 μl pipette tip. After the scratch, the detached cells were removed by gently rinsing 2 times with a medium, and the gap distance was measured as that at 0 h. To determine the cell migration capacity, gap distances were measured 24h and 48h after scoring. The calculation formula of the migration distance is as follows:
migration distance=gap distance at 0 h-gap distance at t (t=24 h or 48 h).
Fig. 9 is a graph of the scratch assay to detect that PANC246 inhibits migration of colorectal cancer cells DLD1 (left panel in fig. 9) and statistical histogram thereof (right panel in fig. 9); * P <0.001; * P <0.0001; control: untransfected control group; pcDNA3.1: empty plasmid transfection sets; PANC246: pcDNA3.1-PANC246 plasmid transfection group.
Fig. 10 is a graph showing that scratch assay detection PANC246 inhibits migration of esophageal cancer cells Eca109 (left panel in fig. 10) and statistical histogram thereof (right panel in fig. 10); * P <0.001; * P <0.0001; control: untransfected control group; pcDNA3.1: empty plasmid transfection sets; PANC246: pcDNA3.1-PANC246 plasmid transfection group.
Fig. 11 is a graph showing that the scratch test detects that PANC246 inhibits migration of liver cancer cells HepG2 (left graph in fig. 11) and a statistical histogram thereof (right graph in fig. 11); * P <0.001; * P <0.0001; control: untransfected control group; pcDNA3.1: empty plasmid transfection sets; PANC246: pcDNA3.1-PANC246 plasmid transfection group.
Fig. 12 is a graph showing that scratch assay detection PANC246 inhibits migration of gastric cancer cell MGC803 (left graph in fig. 12) and statistical histogram thereof (right graph in fig. 12); * P <0.001; * P <0.0001; control: untransfected control group; pcDNA3.1: empty plasmid transfection sets; PANC246: pcDNA3.1-PANC246 plasmid transfection group.
Fig. 13 is a graph of scratch assay detection PANC246 inhibiting migration of colorectal cancer cells SW480 (left panel in fig. 13) and statistical histogram thereof (right panel in fig. 13); * P <0.001; * P <0.0001; control: untransfected control group; pcDNA3.1: empty plasmid transfection sets; PANC246: pcDNA3.1-PANC246 plasmid transfection group.
IV and Transwell cell method for detecting cell invasion capability
Cell invasion capacity assays were performed using a Transwell chamber (Chemicon, usa). Cell suspensions transfected with pcDNA3.1-PANC246, untransfected control and pcDNA3.1 (0.5X10) 5 Individual cells/mL) was added to the Transwell chamber while 200 μl of serum-free medium was added, and 500 μl of medium containing 10% fetal bovine serum was added to the lower chamber as a stimulus for invasive transfer. After the Transwell chamber is placed in a cell incubator for 24 hours, the invasive cells on the lower surface of the chamber membrane are subjected to crystal violet staining for 10 minutes, and photographed under a microscope with 40 times high-power visual field.
Fig. 14 is a graph showing the results of Transwell laboratory experiments to detect the ability of PANC246 to inhibit tumor cell invasion, and fig. 14 shows that tumor cell staining through Transwell cell membranes shows that PANC246 significantly inhibits tumor cell invasion; * P <0.001; * P <0.0001; control: untransfected control group; pcDNA3.1: empty plasmid transfection sets; PANC246: pcDNA3.1-PANC246 plasmid transfection group.
V, apoptosis detection
Cells were trypsinized and washed twice with pre-chilled Phosphate Buffer (PBS). Add 500. Mu.L of binding buffer (KeyGen) and resuspend to give a 5X 10 cell number 5 Individual cells. mu.L of Annexin V-FITC (KeyGen) was added to the cell suspension, and the cell suspension was counterstained with 5. Mu.L of Propidium Iodide (PI). The mixture was incubated for 10min in the dark at room temperature and then subjected to apoptosis analysis using a FlowSight flow cytometer (Merck, germany).
FIG. 8 is a graph showing the results of flow cytometry detection of PANC246 pro-cancer apoptosis in this example, annexin V-FITC staining for early apoptosis, PI staining for late apoptosis; control: untransfected control group; pcDNA3.1: empty plasmid transfection sets; PANC246: pcDNA3.1-PANC246 plasmid transfection group.
VI, fluorescent quantitative PCR
Total RNA was collected using TRIzol (Invitrogen, USA) and converted to cDNA using the first strand cDNA Synthesis kit (Vazyme Biotech, china) according to the instructions. Real-time fluorescent quantitative PCR was performed on an ABI 7500PCR instrument (ABI, usa) using SYBR Green Master Mix (Vazyme Biotech). The GAPDH gene served as an internal reference for this experiment.
VII, PANC246 screening and meta analysis
11,093 gene expression level data were downloaded from the TCGA database (https:// portal. Gdc. Cancer. Gov/repositisource), the data source being transcriptome sequencing (RNA-seq) data. The RNA-seq data initially covered 32 cancer types, but 9 of them were excluded due to the low sample size of the control group. Differential gene expression analysis was performed using the quartile per kilobase log2 transformed fragment (FPKM-UQ) of the HTSeq transcript. Differential gene expression analysis was performed using the Bayesian generalized linear model (Bayesglm) of ARM package (v 1.10-1). Meta analysis was performed on 23 cancer types using Metafor software package (v 2.1-1).
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.
Claims (2)
1. The application of the vector over-expressing PANC246 in preparing the medicine for inhibiting the cancer is characterized in that: the PANC246 is a novel ncRNA encoded by ENSG 00000231246.1.
2. The use according to claim 1, characterized in that: the cancers include esophageal cancer, liver cancer, gastric cancer and colorectal cancer.
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| CN108179194A (en) * | 2018-03-05 | 2018-06-19 | 南通大学附属医院 | A kind of tumor cells marker circBIRC6 and its inhibitor and purposes |
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