Aberrant promoter CpG islands methylation of tumor suppressor genes in cholangiocarcinoma
- Authors
- Uhm, Kyung-Ok; Lee, Eun Soo; Lee, Yun Mi; Kim, Hyeon Soo; Park, Young-Nyun; Park, Sun-Hwa
- Issue Date
- 2008
- Publisher
- COGNIZANT COMMUNICATION CORP
- Keywords
- cholangiocarcinoma; hypermethylation; methylation-specific PCR; tumor suppressor gene
- Citation
- ONCOLOGY RESEARCH, v.17, no.4, pp.151 - 157
- Indexed
- SCIE
SCOPUS
- Journal Title
- ONCOLOGY RESEARCH
- Volume
- 17
- Number
- 4
- Start Page
- 151
- End Page
- 157
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/125581
- DOI
- 10.3727/096504008785114110
- ISSN
- 0965-0407
- Abstract
- Aberrant DNA methylation of 5'-CpG islands located within gene promoters has been identified as a mechanism for transcriptional inactivation of tumor suppressor genes. To ascertain the mechanism of gene promoter hypermethylation in cholangiocarcinoma (CC), we investigated promoter methylation status of the candidate genes ID4, DLC-1, and SFRP1 in 41 CCs, 19 adjacent nontumor tissues, and 15 normal liver tissues using methylation-specific PCR (MSP). The frequencies of DNA methylation were: 57.5% (23 of 40) for ID4, 14.3% (5 of 35) for DLC-1, and 63.4% (26 of 41) for SFRP1, respectively. In contrast, a low frequency of methylation was detected in nontumor tissues. In addition, hypermethylated status of these genes was detected in three kinds of CC cell lines. Moreover, the downregulated expression of these genes in these cells was restored by treatment with 5-aza-2'-deoxycytidine, a DNA methyltransferase inhibitor. Taken together, these results suggest that abet-rant DNA methylation may contribute to the tumorigenesis of cholangiocarcinoma.
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Collections - Graduate School > Department of Biomedical Sciences > 1. Journal Articles
- College of Medicine > Department of Medical Science > 1. Journal Articles
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