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English Abstract
Journal Article
Research Support, Non-U.S. Gov't
[Induction of SMYD3 by hepatitis B virus X gene in HepG2 cells].
Zhonghua Gan Zang Bing za Zhi = Zhonghua Ganzangbing Zazhi = Chinese Journal of Hepatology 2009 April
OBJECTIVE: To explore the role SMYD3 and histone methylation in the carcinogenesis of HBV-related hepatocellular carcinoma (HCC).
METHODS: HBx expressing plasmid was transfected into HepG2 cell, the localization of HBx and SMYD3 was detected by immunofluorescence, SMYD3 mRNA and protein were checked by real-time reverse transcription polymerase chain reaction and western blot, cell proliferation and apoptosis were detected by flow cytometry.
RESULTS: After HBx transfection, HBx and SMYD3 protein were mainly localized in nucleus. HBx protein enhanced SMYD3 mRNA and SMYD3 expressions in HepG2. After HBx transfection, apoptosis of HepG2 was decreased, and cell proliferation was increased.
CONCLUSIONS: HBx may induce the expression of histone methyltransferase SMYD3, which in turn stimulates cell proliferation and blocks apoptosis.
METHODS: HBx expressing plasmid was transfected into HepG2 cell, the localization of HBx and SMYD3 was detected by immunofluorescence, SMYD3 mRNA and protein were checked by real-time reverse transcription polymerase chain reaction and western blot, cell proliferation and apoptosis were detected by flow cytometry.
RESULTS: After HBx transfection, HBx and SMYD3 protein were mainly localized in nucleus. HBx protein enhanced SMYD3 mRNA and SMYD3 expressions in HepG2. After HBx transfection, apoptosis of HepG2 was decreased, and cell proliferation was increased.
CONCLUSIONS: HBx may induce the expression of histone methyltransferase SMYD3, which in turn stimulates cell proliferation and blocks apoptosis.
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