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

Virology Journal

Xiaoming Jin⁴  Zuxi Yu¹  Chong Zhang⁴  Chao Li⁴  Di Wu³  Lei Zhang⁴  Dan Kong²  Yiqi Wu⁴  Ran Zhao⁴  Tianzhen Wang⁴ 

[1] National Heart, Lung and Blood Institute of National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland 20892, USA;Cancer Research Institute of Kanazawa University Kakuma-machi, Kanazawa 920-1192, Japan;Department of Obstetrics and Gynecology, First Affiliated Hospital of Harbin Medical University, Harbin 150001, China;Department of Pathology, Basic Medical Science College, Harbin Medical University, 157 Baojian Road, Nangang District, Harbin 150081, China

关键词: cell cycle;    proliferation;    HBV;    HepG2;    HepG2.2.15;   

Others  :  1156691
DOI  :  10.1186/1743-422X-8-231

 received in 2011-01-21, accepted in 2011-05-15,  发布年份 2011

【 摘 要 】

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.

【 授权许可】

   
2011 Wang et al; licensee BioMed Central Ltd.

【 图 表 】

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