Premium
Expression of tumor suppressor p53 facilitates DNA repair but not UV‐induced G2/M arrest or apoptosis in Chinese hamster ovary CHO‐K1 cells
Author(s) -
Chang YuChing,
Liao ChuBin,
Hsieh PeiYu Chiang,
Liou MingLi,
Liu YinChang
Publication year - 2008
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.21428
Subject(s) - chinese hamster ovary cell , apoptosis , dna damage , microbiology and biotechnology , biology , comet assay , cell cycle , dna repair , transactivation , cell cycle checkpoint , suppressor , chemistry , dna , cell culture , genetics , gene expression , gene
Tumor suppressor p53 is an essential regulator in mammalian cellular responses to DNA damage including cell cycle arrest and apoptosis. Our study with Chinese hamster ovary CHO‐K1 cells indicates that when p53 expression and its transactivation capacity was inhibited by siRNA, UVC‐induced G2/M arrest or apoptosis were unaffected as revealed by flow cyotmetric analyses and other measurements. However, inhibition of p53 rendered the cells slower to repair UV‐induced damages upon a plasmid as shown in host cell reactivation assay. Furthermore, the nuclear extract (NE) of p53 siRNA‐treated cells was inactive to excise the UV‐induced DNA adducts as analyzed by comet assay. Consistently, the immunodepletion of p53 also deprived the excision activity of the NE in the similar experiment. Thus, tumor suppressor p53 of CHO‐K1 cells may facilitate removal of UV‐induced DNA damages partly via its involvement in the repair mechanism. J. Cell. Biochem. 103: 528–537, 2008. © 2007 Wiley‐Liss, Inc.