Epigenetic methylation of TIMP-3 may play a role in HBV-associated hepatocellular carcinoma.
Hepatitis B virus (HBV) infection is highly correlated with hepatocellular carcinoma (HCC) and many molecular mechanisms have been proposed. Based on the new data that HCC cell lines containing the HBV genome mostly show tissue inhibitor of metalloproteinase-3 (TIMP-3) repression on both mRNA and protein levels, and on the result of computer analysis of TIMP-3 gene structure, we proposed an alternative model to explain HBV-induced HCC: TIMP-3 transcription might be silenced by epigenetic methylation.
Lai
Huey-Jen
HJ
Graduate Institute of Basic Medical Sciences, Chang Gung University, Taoyuan, Taiwan.
Lo
Szecheng J
SJ
D023081:CCAAT-Binding Factor / Q000502:physiology; D006528:Carcinoma, Hepatocellular / Q000209:etiology*; D019175:DNA Methylation; D044127:Epigenesis, Genetic; D006509:Hepatitis B / Q000150:complications*; D006801:Humans; D008113:Liver Neoplasms / Q000209:etiology*; D011401:Promoter Regions, Genetic; D019717:Tissue Inhibitor of Metalloproteinase-3 / Q000235:genetics*
D023081:CCAAT-Binding Factor; D019717:Tissue Inhibitor of Metalloproteinase-3