title: HBsAg inhibits the translocation of JTB into mitochondria in HepG2 cells and potentially plays a role in HCC progression.
abstract: OBJECTIVE
  The expression of the jumping translocation breakpoint (JTB) gene is upregulated in malignant liver tissues; however, JTB is associated with unbalanced translocations in many other types of cancer that suppress JTB expression. No comprehensive analysis on its function in human hepatocellular carcinoma (HCC) has been performed to date. We aimed to define the biological consequences for interaction between JTB and HBsAg in HCC cell lines.
  
  
  METHODS
  We employed the stable transfection to establish small HBsAg expressing HepG2 cell line, and stably silenced the JTB expression using short hairpin RNA in HepG2 cell line. The effects of JTB and small HBsAg in vitro were determined by assessing cell apoptosis and motility.
  
  
  RESULTS
  Silencing of JTB expression promoted cancer cell motility and reduced cell apoptosis, which was significantly enhanced by HBs expression. Expression of HBsAg inhibited the translocation of JTB to the mitochondria. Furthermore, silencing of the JTB resulted in an increase in the phosphorylation of p65 in HepG2 cells and HepG2-HBs cells, whereas HBsAg expression decreased the phosphorylation of p65. The silencing of JTB in HepG2-HBs cells conferred increased advantages in cell motility and anti-apoptosis.
  
  
  CONCLUSIONS
  HBsAg inhibited the translocation of JTB to the mitochondria and decreased the phosphorylation of p65 through the interaction with JTB, After JTB knockdown, HBsAg exhibited a stronger potential to promote tumor progression. Our data suggested that JTB act as a tumor suppressor gene in regards to HBV infection and its activation might be applied as a therapeutic strategy for in control of HBV related HCC development.
authors.affiliation: Department of Gastroenterology, Zhongshan Hospital affiliated to Xiamen University, Xiamen, Fujian Province, China.
authors.forename: Yun-Peng
authors.initials: YP
authors.lastname: Liu
authors.forename: Xiao-Ning
authors.initials: XN
authors.lastname: Yang
authors.forename: Amarsanaa
authors.initials: A
authors.lastname: Jazag
authors.forename: Jin-Shui
authors.initials: JS
authors.lastname: Pan
authors.forename: Tian-Hui
authors.initials: TH
authors.lastname: Hu
authors.forename: Jing-Jing
authors.initials: JJ
authors.lastname: Liu
authors.forename: Bayasi
authors.initials: B
authors.lastname: Guleng
authors.forename: Jian-Lin
authors.initials: JL
authors.lastname: Ren
mesh_terms: D017209:Apoptosis / Q000235:genetics; D006528:Carcinoma, Hepatocellular / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics; D018450:Disease Progression; D020868:Gene Silencing; D016147:Genes, Tumor Suppressor; D056945:Hep G2 Cells; D006509:Hepatitis B / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D006514:Hepatitis B Surface Antigens / Q000235:genetics / Q000378:metabolism*; D006515:Hepatitis B virus / Q000235:genetics / Q000378:metabolism; D006801:Humans; D008113:Liver Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D008565:Membrane Proteins / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism*; D008930:Mitochondria, Liver / Q000235:genetics / Q000378:metabolism*; D009363:Neoplasm Proteins / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism*; D010766:Phosphorylation / Q000235:genetics; D034741:RNA, Small Interfering / Q000235:genetics; D014162:Transfection / Q000379:methods; D014178:Translocation, Genetic; D019892:eIF-2 Kinase / Q000235:genetics / Q000378:metabolism
chemical_list: D006514:Hepatitis B Surface Antigens; C407989:JTB protein, human; D008565:Membrane Proteins; D009363:Neoplasm Proteins; D034741:RNA, Small Interfering; D019892:eIF-2 Kinase