Expression deficiency of JWA enhanced DNA damage and delayed DNA repair in HeLa cells induced by benzo (a) pyrene exposure.
- Author:
Zu-long LIU
1
;
Deng-an GU
;
Ai-ping LI
;
Qi-zhan LIU
;
Jian-wei ZHOU
Author Information
- Publication Type:Journal Article
- MeSH: Benzo(a)pyrene; toxicity; DNA Damage; drug effects; DNA Repair; DNA-Formamidopyrimidine Glycosylase; deficiency; genetics; Gene Expression; HeLa Cells; Heat-Shock Proteins; deficiency; genetics; Humans; Intracellular Signaling Peptides and Proteins; deficiency; genetics
- From: Chinese Journal of Preventive Medicine 2006;40(2):84-87
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of JWA gene in benzo (a) pyrene [B (a) P] induced DNA damage and repair effects in HeLa cells.
METHODSThe antisense JWA express vector (pEGFP-C1-asJWA) was constructed and stably transfected into HeLa cells. JWA deficient HeLa cells (asJWA-HeLa) was then screened and established. The general characteristics of asJWA-HeLa cells were investigated. DNA damage and repair cell culture model was conducted by treating the cells with 50 micromol/L B (a) P plus S9 for 3 hours and then the cells were maintained further 0, 1, 3, and 24 hours for DNA repairing. The damaged DNA was detected by single cell gel electrophoresis assay (comet assay).
RESULTSJWA deficient HeLa cells (with a 31% of JWA protein expression as compared with the control) were obtained successfully. Compared with the empty vector transfected cells (C1-HeLa) and the untransfected HeLa cells, asJWA-HeLa cells were more sensitive to B (a) P exposure and with a delayed DNA repair process.
CONCLUSIONThe JWA determined might function as a potential effective environmental responsive gene and actively participate the process of B (a) P exposure associated with intracellular signal pathways of DNA damage and repair.
