Expression of tumor suppressor p53 facilitates DNA repair but not UV-induced G2/M arrest or apoptosis in chinese hamster ovary CHO-K1 cells

被引：18

作者：

Chang, Yu-Ching ^{[1
]}

Liao, Chu-Bin ^{[2
]}

Hsieh, Pei-Yu Chiang ^{[1
]}

Liou, Ming-Li ^{[1
]}

Liu, Yin-Chang ^{[1
,2
]}

机构：

[1] Natl Tsing Hua Univ, Inst Mol Med, Hsinchu 30043, Taiwan

[2] Natl Tsing Hua Univ, Dept Life Sci, Hsinchu 30043, Taiwan

来源：

JOURNAL OF CELLULAR BIOCHEMISTRY | 2008年 / 103卷 / 02期

关键词：

Chinese hamster ovary CHO-K1 cells; UVC; apoptosis; G2/M arrest; caffeine; p53; comet assay; host cell reactivation assay; DNA repair;

D O I：

10.1002/jcb.21428

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Tumor suppressor p53 is an essential regulator in mammalian cellular responses to DNA damage including cell cycle arrest and apoptosis. Ourstudy 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.

引用

页码：528 / 537

页数：10

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