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Promoter hypermethylation regulates UCHL1 expression in cholangiocarcinoma cell lines |
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| รหัสดีโอไอ | |
| Creator | Phatchareeporn Choodetwattana |
| Title | Promoter hypermethylation regulates UCHL1 expression in cholangiocarcinoma cell lines |
| Contributor | Siriporn Proungvitaya, Patcharee Jearanaikoon, Waraporn Chan-on, Temduang Limpaiboon |
| Publisher | Faculty of Associated Medical Sciences, Khon Kaen University, Thailand |
| Publication Year | 2564 |
| Journal Title | Archives of Allied Health Sciences |
| Journal Vol. | 33 |
| Journal No. | 2 |
| Page no. | 1-8 |
| Keyword | Hypermethylation, Silencing, UCHL1, 5-azacytidine |
| URL Website | https://he01.tci-thaijo.org/index.php/ams/about |
| Website title | Archives of Allied Health Sciences (Arch AHS) |
| ISSN | 2730-1990 |
| Abstract | Cholangiocarcinoma (CCA) is a significant health burden in Northeastern Thailand. Aberrant DNA methylation is a characteristic feature of most human cancers. Although overexpression of UCHL1 was observed in primary hilar CCA, the regulation of UCHL1 expression by DNA methylation in CCA has not yet been confirmed. We herein detected DNA methylation and mRNA expression levels in CCA and immortalized cholangiocyte cell lines using MS-HRM and RT-PCR, respectively. The results showed inverse correlation between DNA methylation levels and mRNA expression levels in CCA cell lines. To confirm whether DNA methylation regulated UCHL1 expression in CCA, 5-azacytidine was applied to inhibit DNA methylation process. We found that UCHL1 protein was up-regulated while DNA methylation was reduced after treatment suggesting the regulation of UCHL1 expression by DNA methylation. To study the role of UCHL1, CCA cell lines were transfected with vector harboring UCHL1 gene and control vector. Cell proliferation and chemotherapeutic drug sensitivity were investigated. The results showed no difference between these two groups. Our study reveals that overexpression of UCHL1 alone is not sufficient to neither inhibit tumor cell growth nor enhance chemoresponsiveness. Nevertheless, UCHL1 expression is epigenetically control indicating its function as a tumor suppressor by which the key features of UCHL1 and its partners in CCA are worth investigating. |
