MiRNA expressions in non-cancerous and cancerous human gastric tissues
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE23739 | GEO | 2011/08/01
SECONDARY ACCESSION(S): PRJNA130763
REPOSITORIES: GEO
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Project description:We investigated the involvement of microRNAs (miRNAs) in gastric cancers. MiRNA expression was profiled from 40 cancerous and 40 non-cancerous tissues obtained from the National Cancer Centre, Singapore, and Singhealth Tissue Repository, Singapore. We identified 80 differentially expressed miRNAs in tumors compared with normal tissues. Among these miRNAs, we identified hsa-mir-486-5p (mir-486) as a significantly downregulated miRNA in GC. Subsequent functional characterization revealed that mir-486 playing a tumor suppressor role. We also observed frequent genomic deletion of mir-486 in 20-30% of GCs. To our knowledge, mir-486 represents one of the first tumor suppressor miRNAs in GC inactivated through genomic deletion. MiRNA expression was profiled on Agilent Human miRNA Microarrays (V2) representing 723 human and 76 human viral miRNAs in 40 normal and 40 cancerous gastric tissues.
2011-08-01 | E-GEOD-23739 | biostudies-arrayexpress
Project description:We investigated the involvement of microRNAs (miRNAs) in gastric cancers. MiRNA expression was profiled from 40 cancerous and 40 non-cancerous tissues obtained from the National Cancer Centre, Singapore, and Singhealth Tissue Repository, Singapore. We identified 80 differentially expressed miRNAs in tumors compared with normal tissues. Among these miRNAs, we identified hsa-mir-486-5p (mir-486) as a significantly downregulated miRNA in GC. Subsequent functional characterization revealed that mir-486 playing a tumor suppressor role. We also observed frequent genomic deletion of mir-486 in 20-30% of GCs. To our knowledge, mir-486 represents one of the first tumor suppressor miRNAs in GC inactivated through genomic deletion. MiRNA expression was profiled on Agilent Human miRNA Microarrays (V2) representing 723 human and 76 human viral miRNAs in 40 normal and 40 cancerous gastric tissues.
2015-07-29 | E-GEOD-23739 | ExpressionAtlas
Project description:Identifying biomarkers predictive for early esophageal cancer detection is critical considering the dismal survival rates. We investigated the involvement of microRNAs (miRNAs), their utility as biomarkers, and their association with survival in esophageal cancer, including Barrett’s associated and sporadic adenocarcinoma (ADC), and squamous cell carcinoma (SCC). MiRNA expression was measured in cancerous and adjacent non-cancerous tissue pairs collected from 76 US and Japanese patients enrolled in 3 distinct cohorts. In ADC patients, miR-21, miR-194, miR-293, and miR-223 expression was elevated, while miR-375 and miR-203 expression was reduced in cancerous tissue compared to non-cancerous tissue. Increased levels of miR-192 and miR-194 were observed in Barrett’s associated compared to sporadic ADC cancerous tissue. In SCC patients, miR-21, miR-181b, miR-155, and miR-146b expression was elevated while miR-375 and miR-203 levels were reduced in cancerous tissue compared to non-cancerous tissue. Significantly, elevated mir-21 expression in non-cancerous tissue was strongly associated with worse prognosis, independent of nodal status and age. Sample classification using miRNA expression yielded accuracies as high as 86% for diagnosis and 78% for Barrett’s esophagus status. Our results highlight that miRNAs are deregulated in esophageal carcinogenesis and Barrett’s esophagus, and that their expression is associated with survival in cancer patients. Sample classification using miRNA expression demonstrates their potential utility as biomarkers for esophageal carcinoma diagnosis.
2010-07-09 | GSE13937 | GEO
Project description:Identifying biomarkers predictive for early esophageal cancer detection is critical considering the dismal survival rates. We investigated the involvement of microRNAs (miRNAs), their utility as biomarkers, and their association with survival in esophageal cancer, including Barrett’s associated and sporadic adenocarcinoma (ADC), and squamous cell carcinoma (SCC). MiRNA expression was measured in cancerous and adjacent non-cancerous tissue pairs collected from 76 US and Japanese patients enrolled in 3 distinct cohorts. In ADC patients, miR-21, miR-194, miR-293, and miR-223 expression was elevated, while miR-375 and miR-203 expression was reduced in cancerous tissue compared to non-cancerous tissue. Increased levels of miR-192 and miR-194 were observed in Barrett’s associated compared to sporadic ADC cancerous tissue. In SCC patients, miR-21, miR-181b, miR-155, and miR-146b expression was elevated while miR-375 and miR-203 levels were reduced in cancerous tissue compared to non-cancerous tissue. Significantly, elevated mir-21 expression in non-cancerous tissue was strongly associated with worse prognosis, independent of nodal status and age. Sample classification using miRNA expression yielded accuracies as high as 86% for diagnosis and 78% for Barrett’s esophagus status. Our results highlight that miRNAs are deregulated in esophageal carcinogenesis and Barrett’s esophagus, and that their expression is associated with survival in cancer patients. Sample classification using miRNA expression demonstrates their potential utility as biomarkers for esophageal carcinoma diagnosis. MiRNA microarray expression was measured using miRNA microarray chips version 3 (Ohio State University) in 44 SCC cases and 32 ADC cases, of which 18 were also diagnosed with Barrett’s esophagus.
2010-07-09 | E-GEOD-13937 | biostudies-arrayexpress
Project description:MicroRNAs is a rapidly expanding area expected to change the way in which diseases will be diagnosed, treated and monitored in the future. Hepatocellular carcinoma (HCC) shows a rising incidence with high mortality but lack of effective targeted therapies. We identified the aberrantly expressed miRNAs involved in HCC through the comparison of miRNA expression profiling in cancerous hepatocytes with that in normal primary human hepatocytes and found 37 dysregulated miRNAs in HCC. There were 9 up-regulated miRNAs and 28 down-regulated miRNAs in HCC, of which, miR-221 and miR-99b were the most overexpressed miRNAs, while miR-375, miR-192, miR-146b-5p, miR-885-5p, miR-122* and miR-122 were noted for their greatest changes of decreased expression. These aberrantly expressed miRNAs may provide insights into pathogenesis of HCC and thus may be used for diagnosis and therapy.
2010-12-30 | GSE20077 | GEO
Project description:MicroRNAs (miRNAs, miRs) are small noncoding RNAs, which control or are controlled by the dysregulation of multiple protein-coding oncogenes or tumor suppressor genes, play important roles in carcinogenesis. Myxoid liposarcomas (MLS) are characterized by t(12;16)(q13;p11) translocation and expression of TLS/CHOP chimeric transcripts (various types) which encode different oncogenic proteins. TLS-CHOP is important for the molecular mechanisms in the development of MLS, but the involvement in microRNA expression still remain poorly understood. Thus we explored the target microRNA of TLS-CHOP influence cell-proliferation or cell death with microarray. MicroRNAs (miRNAs, miRs) are small noncoding RNAs, which control or are controlled by the dysregulation of multiple protein-coding oncogenes or tumor suppressor genes, play important roles in carcinogenesis. Myxoid liposarcomas (MLS) are characterized by t(12;16)(q13;p11) translocation and expression of TLS/CHOP chimeric transcripts (various types) which encode different oncogenic proteins. TLS-CHOP is important for the molecular mechanisms in the development of MLS, but the involvement in microRNA expression still remain poorly understood. In this study, we have found that miR-486-5p (miR-486) expression level was downregulated by ectopic expression of TLS-CHOP fusion gene in mouse fibroblast cells (NIH3T3). In addition, we found overexpression of miR-486 inhibited the cell growth in the 2645/94 cells and in situ hybridization of miR-486 showed MLS tissues had lower signal intensity compared with non-tumor tissues. Thus we explored the target genes of miR-486 influence cell-proliferation or cell death with microarray. We compared the microRNA profiles of cells treated with TLS-CHOP or empty vector about NIH-3T3 cell-line. We compared the whole mRNA profiles of cells transfected with miR-486 oligonucleotides or control oligo about myxoid liposarcoma cell-line.
2013-03-23 | E-GEOD-36966 | biostudies-arrayexpress
Project description:We determined the effect of p53 activation on de novo protein synthesis using quantitative proteomics of newly synthesized proteins (pulsed stable isotope labeling with amino acids in cell culture, pSILAC) in combination with mRNA and non-coding RNA expression analyses by next generation sequencing (RNA-, miR-Seq) in the colorectal cancer (CRC) cell line SW480. Furthermore, genome-wide DNA binding of p53 was analyzed by chromatin-immunoprecipitation (ChIP-Seq). Thereby, we identified differentially regulated mRNAs (1258 up, 415 down), miRNAs (111 up, 95 down), lncRNAs (270 up, 123 down) and proteins (542 up, 569 down). Changes in mRNA and protein expression levels showed a positive correlation (r = 0.50, p < 0.0001). More transcriptionally induced genes displayed occupied p53 binding sites (4.3% mRNAs, 7.2% miRNAs, 6.3% lncRNAs, 5.9% proteins) than repressed genes (2.4% mRNAs, 3.2% miRNAs, 0.8% lncRNAs, 1.9% proteins), suggesting indirect mechanisms of repression. Around 50% of the downregulated proteins displayed seed-matching sequences of p53-induced miRNAs in the corresponding 3’-UTRs. Moreover, proteins repressed by p53 significantly overlapped with those previously shown to be repressed by miR-34a. We confirmed upregulation of the novel direct p53 target genes LINC01021, MDFI, ST14 and miR-486 and showed that ectopic LINC01021 expression inhibited proliferation in SW480 cells. Furthermore, HMGB1, KLF12 and CIT mRNAs were confirmed as direct targets of the p53-induced miR-34a, miR-205 and miR-486-5p, respectively. In line with the loss of p53 function during tumor progression, elevated expression of HMGB1, KLF12 and CIT was detected in advanced stages of cancer. This study provides new insights and a comprehensive catalogue of p53-mediated regulations and p53 DNA binding in CRC cells.
2015-07-23 | PXD001976 | Pride
Project description:We determined the effect of p53 activation on de novo protein synthesis using quantitative proteomics of newly synthesized proteins (pulsed stable isotope labeling with amino acids in cell culture, pSILAC) in combination with mRNA and non-coding RNA expression analyses by next generation sequencing (RNA-, miR-Seq) in the colorectal cancer (CRC) cell line SW480. Furthermore, genome-wide DNA binding of p53 was analyzed by chromatin-immunoprecipitation (ChIP-Seq). Thereby, we identified differentially regulated mRNAs (1258 up, 415 down), miRNAs (111 up, 95 down), lncRNAs (270 up, 123 down) and proteins (542 up, 569 down). Changes in mRNA and protein expression levels showed a positive correlation (r = 0.50, p < 0.0001). More transcriptionally induced genes displayed occupied p53 binding sites (4.3% mRNAs, 7.2% miRNAs, 6.3% lncRNAs, 5.9% proteins) than repressed genes (2.4% mRNAs, 3.2% miRNAs, 0.8% lncRNAs, 1.9% proteins), suggesting indirect mechanisms of repression. Around 50% of the downregulated proteins displayed seed-matching sequences of p53-induced miRNAs in the corresponding 3â??-UTRs. Moreover, proteins repressed by p53 significantly overlapped with those previously shown to be repressed by miR-34a. We confirmed upregulation of the novel direct p53 target genes LINC01021, MDFI, ST14 and miR-486 and showed that ectopic LINC01021 expression inhibited proliferation in SW480 cells. Furthermore, HMGB1, KLF12 and CIT mRNAs were confirmed as direct targets of the p53-induced miR-34a, miR-205 and miR-486-5p, respectively. In line with the loss of p53 function during tumor progression, elevated expression of HMGB1, KLF12 and CIT was detected in advanced stages of cancer. This study provides new insights and a comprehensive catalogue of p53-mediated regulations and p53 DNA binding in CRC cells.
2016-05-24 | MSV000079767 | MassIVE
Project description:MicroRNAs (miRNAs, miRs) are small noncoding RNAs, which control or are controlled by the dysregulation of multiple protein-coding oncogenes or tumor suppressor genes, play important roles in carcinogenesis. Myxoid liposarcomas (MLS) are characterized by t(12;16)(q13;p11) translocation and expression of TLS/CHOP chimeric transcripts (various types) which encode different oncogenic proteins. TLS-CHOP is important for the molecular mechanisms in the development of MLS, but the involvement in microRNA expression still remain poorly understood. Thus we explored the target microRNA of TLS-CHOP influence cell-proliferation or cell death with microarray. MicroRNAs (miRNAs, miRs) are small noncoding RNAs, which control or are controlled by the dysregulation of multiple protein-coding oncogenes or tumor suppressor genes, play important roles in carcinogenesis. Myxoid liposarcomas (MLS) are characterized by t(12;16)(q13;p11) translocation and expression of TLS/CHOP chimeric transcripts (various types) which encode different oncogenic proteins. TLS-CHOP is important for the molecular mechanisms in the development of MLS, but the involvement in microRNA expression still remain poorly understood. In this study, we have found that miR-486-5p (miR-486) expression level was downregulated by ectopic expression of TLS-CHOP fusion gene in mouse fibroblast cells (NIH3T3). In addition, we found overexpression of miR-486 inhibited the cell growth in the 2645/94 cells and in situ hybridization of miR-486 showed MLS tissues had lower signal intensity compared with non-tumor tissues. Thus we explored the target genes of miR-486 influence cell-proliferation or cell death with microarray.
2013-03-23 | GSE36966 | GEO
Project description:To clarify the role of micro (mi) RNAs in gastric carcinogenesis, we studied the expression and function of miRNAs in gastric carcinoma (GC) cells. Initially, we performed microarray analysis using total RNA from three human GC cell lines and non-cancerous gastric tissue. Among the down-regulated miRNAs in GC cells,miR-212 expression was decreased in all eight GC cell lines examined and a significant decrease of miR-212 expression in human primary GC tissues was also observed in 6 of 11 cases. Transfection of the precursor miR-212 molecule induced decreased growth of a GC cell line. Using three different databases, methyl-CpG-binding protein MeCP2 was postulated to be a target of miR-212. As seen on reporter assaying, miR-212 repressed the construct with the MECP2 3'-UTR. Ectopic expression of miR-212 repressed expression of the MeCP2 protein,but not the MECP2 mRNA level. These data suggest that down-regulation of miR-212 may be related to gastric carcinogenesis through its target genes, such as MECP2.
2010-02-10 | GSE18880 | GEO