Hepatitis B virus induces G1 phase arrest by regulating cell cycle genes in HepG2.2.15 cells

BACKGROUND: To investigate the effect of HBV on the proliferative ability of host cells and explore the potential mechanism. METHODS: MTT, colony formation assay and tumourigenicity in nude mice were performed to investigate the effect of HBV on the proliferative capability of host cells. In order t...

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Detalles Bibliográficos
Autores principales: Wang, Tianzhen, Zhao, Ran, Wu, Yiqi, Kong, Dan, Zhang, Lei, Wu, Di, Li, Chao, Zhang, Chong, Yu, Zuxi, Jin, Xiaoming
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Research
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3104952/
https://www.ncbi.nlm.nih.gov/pubmed/21575146
http://dx.doi.org/10.1186/1743-422X-8-231
Descripción
Sumario:BACKGROUND: To investigate the effect of HBV on the proliferative ability of host cells and explore the potential mechanism. METHODS: MTT, colony formation assay and tumourigenicity in nude mice were performed to investigate the effect of HBV on the proliferative capability of host cells. In order to explore the potential mechanism, cell cycle and apoptosis were analysed. The cell cycle genes controlling the G1/S phase transition were detected by immunohistochemistry, westernblot and RT-PCR. RESULTS: HepG2.2.15 cells showed decreased proliferation ability compared to HepG2 cells. G1 phase arrest was the main cause but was not associated with apoptosis. p53, p21 and total retinoblastoma (Rb) were determined to be up-regulated, whereas cyclinE was down-regulated at both the protein and mRNA levels in HepG2.2.15 cells. The phosphorylated Rb in HepG2.2.15 cells was decreased. CONCLUSIONS: Our results suggested that HBV inhibited the capability of proliferation of HepG2.2.15 cells by regulating cell cycle genes expression and inducing G1 arrest.

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