Hepatitis C virus Core protein overcomes all-trans retinoic acid-induced cell growth arrest by inhibiting retinoic acid receptor-beta(2) expression via DNA methylation
- Authors
- Lee, Hyehyeon; Woo, Young-Ju; Kim, Soo Shin; Kim, Sung-Hyun; Park, Bum-Joon; Choi, Dong ho; Jang, Kyung Lib
- Issue Date
- Jul-2013
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- All-trans retinoic acid; DNA methylation; HCV Core; Retinoic acid receptor-beta(2); p16
- Citation
- CANCER LETTERS, v.335, no.2, pp.372 - 379
- Indexed
- SCIE
SCOPUS
- Journal Title
- CANCER LETTERS
- Volume
- 335
- Number
- 2
- Start Page
- 372
- End Page
- 379
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/162327
- DOI
- 10.1016/j.canlet.2013.02.057
- ISSN
- 0304-3835
- Abstract
- Aberrant promoter methylation of tumor suppressor genes including retinoic acid receptor-beta(2) (RAR-beta(2)) is frequently detected in hepatitis C virus (HCV)-associated hepatocellular carcinoma; however, the mechanism and its significance are relatively unknown. Here, we showed that HCV Core induced promoter hypermethylation of RAR-beta(2) to inhibit its expression via up-regulation of DNA methyltransferases 1 and 3b. Under the condition, all-trans retinoic acid (ATRA) failed to activate p16 expression and thus could not inactivate the Rb-E2F pathway. Accordingly, Core-expressing cells exhibited resistance to ATRA-induced growth inhibition. Taken together, HCV Core antagonizes ATRA, a natural anti-cancer compound, to stimulate cell growth via epigenetic down-regulation of RAR-beta(2).
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