| Summary: | 碩士 === 輔仁大學 === 生命科學系碩士班 === 95 === Lung cancer is currently the leading cause of cancer death worldwide as well as in Taiwan. Adenocarcinoma is the most prevalent histological type among female lung cancer. It was noticed that 85 percent of female adenocarcinoma patients are nonsmokers, indicating their higher risks may as least, in part, impute to their distinctive genome. As epigenetic mechanism, such as DNA methylation, has been implicated in regulation of tumor suppressor genes, we therefore analyze whether DNA methylation is the mechanism that affect the gene which is down-regulated in female lung adenocarcinoma. By analyzing microarray profiling of tissue pair from 18 lung adenocarcinoma patients, eight genes including FAM134B, MOSC2, PTPRM, CXCL5, KIAA0256, GPRC5A, EDNRB, and PDPN have been found to down regulated in lung cancer tissue as compared with adjacent normal part. In attempt to analyze whether these genes have CpG islands and display hypermethylation pattern, we used sodium bisulfite conversion method to treat genomic DNA and to sequence the putative CpG island of each gene. After analyzed the methylation status of CpG islands of these genes in one normal lung fibroblast, IMR90, and fourteen lung cancer cell lines, we have found MOSC2, CXCL5 and EDNRB displayed hypermethylation in many lung cancer cell lines as compared to IMR90. In addition, DNA methyltransferase inhibitor, 5-aza-2’-deoxycitidine, can revert their down regulation in a dose dependent manner, indicating DNA methylation may indeed the mechanism that down-regulates the expression of MOSC2, CXCL5 and EDNRB in lung cancer cell lines.
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