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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.

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Related in: MedlinePlus

Morphological features. (A) Morphological feature under inverted microscope. The magnification is 400×. HepG2.2.15 cell line grew in multilayer and adherence. HepG2 cell line grew in monolayer and adherence. (B) Ultrastructural characteristic. Bar, 500 nm. (i) HepG2.2.15 cell (×3000). (ii) Virus inclusion in HepG2.2.15 cell (×15 k). Bottom left is further magnification (×30 k). (iii) HepG2 cell (×6000).
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Figure 1: Morphological features. (A) Morphological feature under inverted microscope. The magnification is 400×. HepG2.2.15 cell line grew in multilayer and adherence. HepG2 cell line grew in monolayer and adherence. (B) Ultrastructural characteristic. Bar, 500 nm. (i) HepG2.2.15 cell (×3000). (ii) Virus inclusion in HepG2.2.15 cell (×15 k). Bottom left is further magnification (×30 k). (iii) HepG2 cell (×6000).

Mentions: HepG2.2.15 cells grew in multiple adherent layers in in vitro culture (Figure 1A) and adhered to the wall of the culture vessel within 24 h and by passage 1 to 2 on days 4-5. HepG2 cells grew in an adherent monolayer with polygonal morphology (Figure 1A) and grew faster than HepG2.2.15 cells where they adhered to the wall of the culture vessel after 2 h and by passage 1 to 2 after 2 days.


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)

Morphological features. (A) Morphological feature under inverted microscope. The magnification is 400×. HepG2.2.15 cell line grew in multilayer and adherence. HepG2 cell line grew in monolayer and adherence. (B) Ultrastructural characteristic. Bar, 500 nm. (i) HepG2.2.15 cell (×3000). (ii) Virus inclusion in HepG2.2.15 cell (×15 k). Bottom left is further magnification (×30 k). (iii) HepG2 cell (×6000).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: Morphological features. (A) Morphological feature under inverted microscope. The magnification is 400×. HepG2.2.15 cell line grew in multilayer and adherence. HepG2 cell line grew in monolayer and adherence. (B) Ultrastructural characteristic. Bar, 500 nm. (i) HepG2.2.15 cell (×3000). (ii) Virus inclusion in HepG2.2.15 cell (×15 k). Bottom left is further magnification (×30 k). (iii) HepG2 cell (×6000).
Mentions: HepG2.2.15 cells grew in multiple adherent layers in in vitro culture (Figure 1A) and adhered to the wall of the culture vessel within 24 h and by passage 1 to 2 on days 4-5. HepG2 cells grew in an adherent monolayer with polygonal morphology (Figure 1A) and grew faster than HepG2.2.15 cells where they adhered to the wall of the culture vessel after 2 h and by passage 1 to 2 after 2 days.

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