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
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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