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

Wang T, Zhao R, Wu Y, Kong D, Zhang L, Wu D, Li C, Zhang C, Yu Z, Jin X - Virol. J. (2011)

Bottom Line: To investigate the effect of HBV on the proliferative ability of host cells and explore the potential mechanism.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pathology, Basic Medical Science College, Harbin Medical University, 157 Baojian Road, Nangang District, Harbin 150081, China.

ABSTRACT

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.

Show MeSH

Related in: MedlinePlus

Cell cycle and apoptosis assay. (A) Cell cycle analysis by FACS. The majority of HepG2.2.15 cells arrested in G1 phase. (B) Cell apoptosis assay by TUNEL. Little cells were apoptotic.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3104952&req=5

Figure 3: Cell cycle and apoptosis assay. (A) Cell cycle analysis by FACS. The majority of HepG2.2.15 cells arrested in G1 phase. (B) Cell apoptosis assay by TUNEL. Little cells were apoptotic.

Mentions: The percentage of cells in each phase of the cell cycle was determined for HepG2.2.15 and HepG2 cells grown in vitro (Table 2). The proportion of cells in G1 phase increased, whereas cells in S phase decreased in HepG2.2.15 compared to HepG2 cells (Figure 3A). HepG2.2.15 cell cycle was arrested at the G1 phase. Apoptosis was determined by TUNEL assay (Figure 3B). The apoptotic rates were low and there was no significant difference observed for HepG2.2.15 and HepG2 cell line.


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

Wang T, Zhao R, Wu Y, Kong D, Zhang L, Wu D, Li C, Zhang C, Yu Z, Jin X - Virol. J. (2011)

Cell cycle and apoptosis assay. (A) Cell cycle analysis by FACS. The majority of HepG2.2.15 cells arrested in G1 phase. (B) Cell apoptosis assay by TUNEL. Little cells were apoptotic.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3104952&req=5

Figure 3: Cell cycle and apoptosis assay. (A) Cell cycle analysis by FACS. The majority of HepG2.2.15 cells arrested in G1 phase. (B) Cell apoptosis assay by TUNEL. Little cells were apoptotic.
Mentions: The percentage of cells in each phase of the cell cycle was determined for HepG2.2.15 and HepG2 cells grown in vitro (Table 2). The proportion of cells in G1 phase increased, whereas cells in S phase decreased in HepG2.2.15 compared to HepG2 cells (Figure 3A). HepG2.2.15 cell cycle was arrested at the G1 phase. Apoptosis was determined by TUNEL assay (Figure 3B). The apoptotic rates were low and there was no significant difference observed for HepG2.2.15 and HepG2 cell line.

Bottom Line: To investigate the effect of HBV on the proliferative ability of host cells and explore the potential mechanism.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pathology, Basic Medical Science College, Harbin Medical University, 157 Baojian Road, Nangang District, Harbin 150081, China.

ABSTRACT

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.

Show MeSH
Related in: MedlinePlus