HBsAg Inhibits the Translocation of JTB into Mitochondria in HepG2 Cells and Potentially Plays a Role in HCC Progression
Autor: | Jian-Lin Ren, Tianhui Hu, Bayasi Guleng, Yun-Peng Liu, Jing-Jing Liu, Amarsanaa Jazag, Xiao-Ning Yang, Jin-Shui Pan |
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Rok vydání: | 2012 |
Předmět: |
Economic growth
HBsAg Gastroenterology and hepatology Tumor Physiology lcsh:Medicine Apoptosis Mitochondria Liver Translocation Genetic Hepatitis eIF-2 Kinase Cell Movement Molecular Cell Biology Basic Cancer Research Genes Tumor Suppressor Phosphorylation RNA Small Interfering lcsh:Science Multidisciplinary Liver Neoplasms virus diseases Hep G2 Cells Signaling in Selected Disciplines Hepatitis B Neoplasm Proteins Infectious hepatitis Oncology Hepg2 cells Disease Progression Medicine Infectious diseases Research Article Signal Transduction Hepatitis B virus Carcinoma Hepatocellular Viral diseases Biology Transfection Hepatitis b surface antigen Cell Line Tumor Gastrointestinal Tumors Humans Gene Silencing Technology Plan Genes tumor suppressor China Liver diseases Oncogenic Signaling Hepatitis B Surface Antigens lcsh:R Disease progression Membrane Proteins Cancers and Neoplasms Hepatocellular Carcinoma Cell movement Virology digestive system diseases lcsh:Q |
Zdroj: | PLoS ONE PLoS ONE, Vol 7, Iss 5, p e36914 (2012) |
ISSN: | 1932-6203 |
Popis: | BACKGROUND AND AIMS: 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. CONCLUSION: 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. |
Databáze: | OpenAIRE |
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