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자료유형
학술저널
저자정보
Liu, Wei-Jun (Department of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital, Wuhan University) Ren, Jian-Guo (Department of Surgery, Huangshi Fourth Hospital) Li, Ting (Department of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital, Wuhan University) Yu, Guo-Zheng (Department of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital, Wuhan University) Zhang, Jin (Department of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital, Wuhan University) Li, Chang-Sheng (Department of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital, Wuhan University) Liu, Zhi-Su (Department of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital, Wuhan University) Liu, Quan-Yan (Department of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital, Wuhan University)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제14권 제11호
발행연도
2013.1
수록면
6,433 - 6,438 (6page)

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In hepatocellular cancer (HCC), lack of response to chemotherapy and radiation treatment can be caused by a loss of epigenetic modifications of cancer cells. Methionine adenosyltransferase 1A is inactivated in HCC and may be stimulated by an epigenetic change involving promoter hypermethylation. Therefore, drugs releasing epigenetic repression have been proposed to reverse this process. We studied the effect of the demethylating reagent 5-aza-2'-deoxycitidine (5-Aza-CdR) on MAT1A gene expression, DNA methylation and S-adenosylmethionine (SAMe) production in the HCC cell line Huh7. We found that MAT1A mRNA and protein expression were activated in Huh7 cells with the treatment of 5-Aza-CdR; the status of promoter hypermethylation was reversed. At the same time, MAT2A mRNA and protein expression was significantly reduced in Huh7 cells treated with 5-Aza-CdR, while SAMe production was significantly induced. However, 5-Aza-CdR showed no effects on MAT2A methylation. Furthermore, 5-Aza-CdR inhibited the growth of Huh7 cells and induced apoptosis and through down-regulation of Bcl-2, up-regulation of Bax and caspase-3. Our observations suggest that 5-Aza-CdR exerts its anti-tumor effects in Huh7 cells through an epigenetic change involving increased expression of the methionine adenosyltransferase 1A gene and induction of S-adenosylmethionine production.

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