
DOI . ORG {
}
Title[redir]:
miR-137 Is Frequently Down-Regulated in Gastric Cancer and Is a Negative Regulator of Cdc42 | Digestive Diseases and Sciences
Description:
Introduction MicroRNAs (miRNAs) are a class of small (19ā25 nucleotides) noncoding RNAs that regulate the expressions of a wide variety of genes, including some involved in cancer development. Some recent studies show that DNA methylation contributes to down-regulation of microRNA-137 (miR-137) during tumorigenesis. Whether down-regulation of miR-137 also exists in gastric cancer is unknown. Aim Our aim was to test the hypothesis that down-regulation of miR-137 also exists in gastric cancer. Methods Expression of levels of miR-137 were examined using real-time PCR on paired gastric cancer and adjacent non-cancerous tissues. The methylation status is detected by MSP. Results Results show that miR-137 is downregulated by hypermethylation of the promoter in gastric cancer tissues. Epigenetic silencing of miR-137 induced an up-regulation of its targets, Cdc42. Restoration of the miR-137 expression in gastric cancer cell lines downregulated the Cdc42 expression. Restoration of the miR-137 and inactivation of Cdc42 induce apoptosis and cell cycle G1 arrest in gastric cancer cells. Furthermore, the miR-137 expression was found to be inversely correlated with CDC42 expression in gastric caner. Conclusions miR-137 is frequently down-regulated in gastric cancer and is a negative regulator of Cdc42.
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Keywords {š}
cancer, article, cdc, gastric, pubmed, google, scholar, cas, chen, cell, expression, access, zhang, res, privacy, cookies, content, downregulated, micrornas, cells, information, publish, search, methylation, downregulation, microrna, epigenetic, open, biol, zhengzhou, data, log, journal, research, frequently, negative, regulator, january, qingjiang, xiaobing, mingzhi, small, dna, hypermethylation, targets, lines, tumor, discover, control, liu,
Topics {āļø}
suxia luoĀ &Ā xinguang cao month download article/chapter raf-mek-erk cascade article digestive diseases tumor-suppressive micrornas silenced related subjects full article pdf dna methylation contributes gastric cancer cells melanoma cell lines paired gastric cancer privacy choices/manage cookies gastric cancer tissues internal medicine-oncology squamous cell carcinoma nat rev cancer mouse reveals delayed mol biol cell mol cell biol henan cancer hospital colorectal cancer cells glioblastoma multiforme cells affiliated cancer hospital european economic area recent studies show real-time pcr body mass index cd11b integrin signaling electronic supplementary material demethylation agent dac promotes cell death clin cancer res conditions privacy policy gastric cancer cdc42-interacting protein-4 noncoding rnas check access instant access microrna-137 promoter methylation dna hypermethylation accepting optional cookies cdc42 induce apoptosis article chen microrna-137 targets microphthalmia medicine-oncology article log author information authors bmc med western blot analysis journal finder publish
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headline:miR-137 Is Frequently Down-Regulated in Gastric Cancer and Is a Negative Regulator of Cdc42
description:MicroRNAs (miRNAs) are a class of small (19ā25 nucleotides) noncoding RNAs that regulate the expressions of a wide variety of genes, including some involved in cancer development. Some recent studies show that DNA methylation contributes to down-regulation of microRNA-137 (miR-137) during tumorigenesis. Whether down-regulation of miR-137 also exists in gastric cancer is unknown. Our aim was to test the hypothesis that down-regulation of miR-137 also exists in gastric cancer. Expression of levels of miR-137 were examined using real-time PCR on paired gastric cancer and adjacent non-cancerous tissues. The methylation status is detected by MSP. Results show that miR-137 is downregulated by hypermethylation of the promoter in gastric cancer tissues. Epigenetic silencing of miR-137 induced an up-regulation of its targets, Cdc42. Restoration of the miR-137 expression in gastric cancer cell lines downregulated the Cdc42 expression. Restoration of the miR-137 and inactivation of Cdc42 induce apoptosis and cell cycle G1 arrest in gastric cancer cells. Furthermore, the miR-137 expression was found to be inversely correlated with CDC42 expression in gastric caner. miR-137 is frequently down-regulated in gastric cancer and is a negative regulator of Cdc42.
datePublished:2011-01-08T00:00:00Z
dateModified:2011-01-08T00:00:00Z
pageStart:2009
pageEnd:2016
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keywords:
miR-137
Gastric cancer
Hypermethylation
Cdc42
Gastroenterology
Hepatology
Oncology
Transplant Surgery
Biochemistry
general
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headline:miR-137 Is Frequently Down-Regulated in Gastric Cancer and Is a Negative Regulator of Cdc42
description:MicroRNAs (miRNAs) are a class of small (19ā25 nucleotides) noncoding RNAs that regulate the expressions of a wide variety of genes, including some involved in cancer development. Some recent studies show that DNA methylation contributes to down-regulation of microRNA-137 (miR-137) during tumorigenesis. Whether down-regulation of miR-137 also exists in gastric cancer is unknown. Our aim was to test the hypothesis that down-regulation of miR-137 also exists in gastric cancer. Expression of levels of miR-137 were examined using real-time PCR on paired gastric cancer and adjacent non-cancerous tissues. The methylation status is detected by MSP. Results show that miR-137 is downregulated by hypermethylation of the promoter in gastric cancer tissues. Epigenetic silencing of miR-137 induced an up-regulation of its targets, Cdc42. Restoration of the miR-137 expression in gastric cancer cell lines downregulated the Cdc42 expression. Restoration of the miR-137 and inactivation of Cdc42 induce apoptosis and cell cycle G1 arrest in gastric cancer cells. Furthermore, the miR-137 expression was found to be inversely correlated with CDC42 expression in gastric caner. miR-137 is frequently down-regulated in gastric cancer and is a negative regulator of Cdc42.
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pageStart:2009
pageEnd:2016
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miR-137
Gastric cancer
Hypermethylation
Cdc42
Gastroenterology
Hepatology
Oncology
Transplant Surgery
Biochemistry
general
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