Human Papilloma Virus Type 16 E7 Oncoprotein Stabilizes p53 Protein but not Induced p53-mediated Apoptosis in HepG2 Cells after gamma-irradiation under Hypoxia.
- Author:
Hye Jin HWANG
1
;
Eun Jung CHOI
;
Yoon Jung CHOI
;
Won Taek LEE
;
Kyung Ah PARK
;
Jong Eun LEE
Author Information
1. Department of Anatomy, Yonsei University College of Medicine, Seoul, Korea. jelee@yumc.yonsei.ac.kr
- Publication Type:Original Article
- Keywords:
E6;
E7;
p53;
HepG2;
Apoptosis;
Hypoxia;
Ionizing radiation
- MeSH:
Anoxia*;
Apoptosis*;
Caspase 3;
Cell Death;
G1 Phase Cell Cycle Checkpoints;
Hep G2 Cells*;
Human papillomavirus 16;
Humans*;
Oncogene Proteins;
Papilloma*;
Radiation, Ionizing
- From:Korean Journal of Anatomy
2007;40(2):95-106
- CountryRepublic of Korea
- Language:English
-
Abstract:
Human papilloma virus 16 E6 and E7 oncoproteins are well known to change cell functions, especially through p53 and pRb expression, so we studied their effects on molecular mechanisms and on the cell death associated with hypoxia and ionizing radiation. These treatments both caused cell death and increased p53 protein expression in HepG2 cells. This increased p53 expression by gamma-irradiation under hypoxia induced G1 cell cycle arrest and led to apoptosis even though HepG2 cells have a relatively reduced ability to induce p21 and pRb expression levels. Ablation of p53 expression by the HPV 16 E6 gene induced E2F-1 expression, which plays a role in cellular survival, especially under hypoxia or gamma-irradiation. The steady-state level of p53 action produced by HPV 16 E7 did not induce apoptotic cell death or the production of the apoptotic regulators, the bcl-2 family and caspase-3, so it did not appear to participate in apoptotic signaling in response to hypoxia and ionizing radiation. Thus, the HPV 16 E7 oncoprotein did not increase the rate of cell death induced by p53, although p53 might play a role in apoptosis in HepG2 cells.
