Regulatory mechanism and target genes of miR-34c in nasopharyngeal carcinoma
碩士 === 長庚大學 === 基礎醫學研究所 === 96 === We used Q-RT-PCR to explore microRNA (miRNA) expression level in NPC tissues. Compared with the normal tissues, miR-34c is down-regulated in NPC tumor tissues. In order to study the targets and biological functions, we overexpressed miR-34c in NPC cells and perform...
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ndltd-TW-096CGU053250512016-05-13T04:15:02Z http://ndltd.ncl.edu.tw/handle/34901898358161120064 Regulatory mechanism and target genes of miR-34c in nasopharyngeal carcinoma 鼻咽癌中microRNA-34c的調控機制以及發覺其所調控的基因 Jhong Syuan Liu 劉忠軒 碩士 長庚大學 基礎醫學研究所 96 We used Q-RT-PCR to explore microRNA (miRNA) expression level in NPC tissues. Compared with the normal tissues, miR-34c is down-regulated in NPC tumor tissues. In order to study the targets and biological functions, we overexpressed miR-34c in NPC cells and performed microarray to detect differentially expressed genes. Microarray analysis detected 846 genes differentially expressing in NPC cells overexpressing miR-34c. TargetScan and miRBase were used to predict potential miR-34c binding sites on the 3’UTR in these genes. Biological functions of individual genes were extracted from OMIM database. Eight candidates which contained potential miR-34c binding sites and were involved in cell cycle control or tumorgenesis were selected and six candidates were validated with Q-PCR. Previous studies have shown that miR-34s expression is down-regulated when p53 signaling is disrupted. However, p53 pathway is intact in most NPC tumors and cell lines. We identified a CpG island in the promoter region of miR-34b/c and found that the CpG island is hypermethylated in three NPC cell lines. Treatment with 5-aza-2’-deoxycytidine(DAC) restored the expression of miR-34c, suggesting that promoter methylation may provide an additional regulatory mechanism for miR-34s expression. J. S. Yu 余兆松 2008 學位論文 ; thesis 71 |
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碩士 === 長庚大學 === 基礎醫學研究所 === 96 === We used Q-RT-PCR to explore microRNA (miRNA) expression level in NPC tissues. Compared with the normal tissues, miR-34c is down-regulated in NPC tumor tissues. In order to study the targets and biological functions, we overexpressed miR-34c in NPC cells and performed microarray to detect differentially expressed genes. Microarray analysis detected 846 genes differentially expressing in NPC cells overexpressing miR-34c. TargetScan and miRBase were used to predict potential miR-34c binding sites on the 3’UTR in these genes. Biological functions of individual genes were extracted from OMIM database. Eight candidates which contained potential miR-34c binding sites and were involved in cell cycle control or tumorgenesis were selected and six candidates were validated with Q-PCR. Previous studies have shown that miR-34s expression is down-regulated when p53 signaling is disrupted. However, p53 pathway is intact in most NPC tumors and cell lines. We identified a CpG island in the promoter region of miR-34b/c and found that the CpG island is hypermethylated in three NPC cell lines. Treatment with 5-aza-2’-deoxycytidine(DAC) restored the expression of miR-34c, suggesting that promoter methylation may provide an additional regulatory mechanism for miR-34s expression.
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author2 |
J. S. Yu |
author_facet |
J. S. Yu Jhong Syuan Liu 劉忠軒 |
author |
Jhong Syuan Liu 劉忠軒 |
spellingShingle |
Jhong Syuan Liu 劉忠軒 Regulatory mechanism and target genes of miR-34c in nasopharyngeal carcinoma |
author_sort |
Jhong Syuan Liu |
title |
Regulatory mechanism and target genes of miR-34c in nasopharyngeal carcinoma |
title_short |
Regulatory mechanism and target genes of miR-34c in nasopharyngeal carcinoma |
title_full |
Regulatory mechanism and target genes of miR-34c in nasopharyngeal carcinoma |
title_fullStr |
Regulatory mechanism and target genes of miR-34c in nasopharyngeal carcinoma |
title_full_unstemmed |
Regulatory mechanism and target genes of miR-34c in nasopharyngeal carcinoma |
title_sort |
regulatory mechanism and target genes of mir-34c in nasopharyngeal carcinoma |
publishDate |
2008 |
url |
http://ndltd.ncl.edu.tw/handle/34901898358161120064 |
work_keys_str_mv |
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