title: Hepatitis B virus X protein mutant upregulates CENP-A expression in             hepatoma cells.
abstract: The carcinogenic role of hepatitis B virus x protein (HBx) in hepatocellular             carcinoma (HCC) remains largely unknown. Centromere protein A (CENP-A) has been             found to be frequently overexpressed in HCC. In the present study, we aimed to             investigate the role of HBx in regulating CENP-A activity in HCC carcinogenesis.             CENP-A expression was examined and the HBx gene was sequenced in 20 HBsAg-positive             HCC patients and corresponding non-cancerous liver tissues. The influence of HBx             mutants on CENP-A expression in HepG2 cells was analyzed by a series of assays.             We found that CENP-A expression was significantly elevated in HCC tissues. HBx             deletion, especially the COOH-terminal deletion of HBx is a frequent event in             HBV-associated HCC tissues. A positive correlation was found between CENP-A expression             and HBx COOH mutation in HCC tissues. HBx mutant increased the expression of the             CENP-A mRNA and protein compared with full-length HBx. However, HBx did not directly             interact with CENP-A. It is concluded that overexpression of CENP-A is closely             associated with HBx COOH mutation in HCC. HBx mutant can increase CENP-A expression,             probably through a mechanism independent of their physical combination, and thereby             it may represent a potential therapeutic strategy for HCC.
authors.affiliation: Department of Pathology, Changhai Hospital, Second Military Medical University, Shanghai 200433, PR China.
authors.forename: Lina
authors.initials: L
authors.lastname: Liu
authors.forename: Yongmei
authors.initials: Y
authors.lastname: Li
authors.forename: Shuhui
authors.initials: S
authors.lastname: Zhang
authors.forename: Danghui
authors.initials: D
authors.lastname: Yu
authors.forename: Minghua
authors.initials: M
authors.lastname: Zhu
mesh_terms: D000328:Adult; D000368:Aged; D001324:Autoantigens / Q000096:biosynthesis*; D001483:Base Sequence; D015153:Blotting, Western; D006528:Carcinoma, Hepatocellular / Q000235:genetics / Q000378:metabolism / Q000821:virology*; D045744:Cell Line, Tumor; D000076247:Centromere Protein A; D002868:Chromosomal Proteins, Non-Histone / Q000096:biosynthesis*; D005260:Female; D056945:Hep G2 Cells; D006801:Humans; D007150:Immunohistochemistry; D047468:Immunoprecipitation; D008113:Liver Neoplasms / Q000235:genetics / Q000378:metabolism / Q000821:virology*; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D009154:Mutation; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015534:Trans-Activators / Q000235:genetics* / Q000378:metabolism; D015854:Up-Regulation; D054334:Viral Regulatory and Accessory Proteins
chemical_list: D001324:Autoantigens; C000619700:CENPA protein, human; D000076247:Centromere Protein A; D002868:Chromosomal Proteins, Non-Histone; D015534:Trans-Activators; D054334:Viral Regulatory and Accessory Proteins; C057628:hepatitis B virus X protein