https://scholars.lib.ntu.edu.tw/handle/123456789/473440
標題: | Differential DNA methylation associated with hepatitis B virus infection in hepatocellular carcinoma | 作者: | Su P.-F. Lee T.-C. Lin P.-J. PO-HUANG LEE YUNG-MING JENG CHIEN-HUNG CHEN JA-DER LIANG Chiou L.-L. GUAN-TARN HUANG Lee, Hsuan-Shu |
公開日期: | 2007 | 卷: | 121 | 期: | 6 | 起(迄)頁: | 1257-1264 | 來源出版物: | International Journal of Cancer | 摘要: | Gene inactivation through DNA hypermethylation plays a pivotal role in carcinogenesis. This study aimed to profile aberrant DNA methylation in different stages of liver disease, namely noncirrhosis, cirrhosis and hepatocellular carcinoma (HCC), and also to clarify the influence of hepatitis B virus (HBV) infection on the aberrant DNA methylation in HCCs. Promoter methylation in p14ARF, p16INK4a, O6- methylguanine-DNA methyltransferase (MGMT), glutathione S-transferase pi (GSTP1) and E-cadherin (E-Cad) genes of 58 HCCs paired with adjacent nontumorous tissues was assayed by methylation-specific PCR. HBV infection was determined using a hepatitis B virus surface antigen (HBsAg) serological assay. The frequency of p16INK4a promoter methylation increased from noncirrhotic, cirrhotic, to HCC tissues (noncirrhotic vs. HCC, p < 0.001), while that of GSTP1 promoter methylation increased in cirrhotic tissues compared to noncirrhotic ones (p = 0.029). The frequency of GSTP1 promoter hypermethylation is significantly higher in HCC than in nontumorous tissues (p = 0.022) from HBsAg-positive patients, but not the HBsAg-negative controls (p = 0.289). While the frequency of E-Cad promoter hypermethylation remained high in both nontumorous tissues and HCCs from HBsAg-positive patients (p = 0.438), it was lower in HCCs than in nontumorous tissues from HBsAg-negative patients (p = 0.002). In contrast, the frequency of p16INK4a, MGMT and p14 ARF promoter hypermethylation in HCCs was unrelated to HBsAg status. In conclusion, aberrant DNA methylation may begin at different stages of liver disease in a gene-dependent manner. Moreover, HBV infection may enhance or maintain GSTP1 and E-Cad promoter methylation and thereby affect hepatocarcinogenesis. ? 2007 Wiley-Liss, Inc. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-34548090762&doi=10.1002%2fijc.22849&partnerID=40&md5=6cafcfe28d50f4c654c0c8c13099296a https://scholars.lib.ntu.edu.tw/handle/123456789/473440 |
ISSN: | 0020-7136 | DOI: | 10.1002/ijc.22849 | SDG/關鍵字: | DNA; glutathione transferase P1; hepatitis B surface antigen; methylated DNA protein cysteine methyltransferase; protein p14ARF; protein p16INK4a; uvomorulin; article; controlled study; DNA methylation; gene inactivation; hepatitis B; Hepatitis B virus; human; human tissue; liver carcinogenesis; liver cell carcinoma; liver cirrhosis; polymerase chain reaction; priority journal; promoter region; Adult; Aged; Aged, 80 and over; Cadherins; Carcinoma, Hepatocellular; DNA Methylation; DNA Modification Methylases; DNA Repair Enzymes; Female; Gene Expression; Genes, p16; Glutathione S-Transferase pi; Hepatitis B; Humans; Immunohistochemistry; Liver Cirrhosis; Liver Neoplasms; Male; Middle Aged; Polymerase Chain Reaction; Promoter Regions (Genetics); Retinoblastoma Protein; Tumor Suppressor Protein p14ARF; Tumor Suppressor Proteins |
顯示於: | 病理學科所 |
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