ARF triggers cell G1 arrest by a P53 independent ERK pathway

被引：3
|
作者：
Du, Hansong [2 ]
Yao, Weiqi [1 ]
Fang, Min [1 ]
Wu, Dongcheng [1 ]
机构：
[1] Wuhan Univ, Basic Med Coll, Dept Biochem, Wuhan 430071, Peoples R China
[2] Huazhong Univ Sci & Technol, Dept Gastrointestinal Surg, Union Hosp, Tongji Med Coll, Wuhan 430074, Peoples R China
来源：
MOLECULAR AND CELLULAR BIOCHEMISTRY | 2011年 / 357卷 / 1-2期
关键词：
ARF; P53; G1; arrest; ERK; TUMOR-SUPPRESSOR; P53-INDEPENDENT APOPTOSIS; ARF/P53; PATHWAY; CYCLE ARREST; P19(ARF); GROWTH; PROLIFERATION; ACTIVATION; P14(ARF); PHOSPHORYLATION;
D O I：
10.1007/s11010-011-0912-4
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
In this study, in order to investigate the p53-independent function of p14ARF, we established p14ARF-inducible clones in the p53-deficient HCT cell line using the doxycycline-inducible expression system. A strong cell growth inhibition and G1/S arrest were observed after doxycycline induction in p53-/-HCT cells, and the cells also exhibited an obvious decrease of DNA synthesis. We further examined if the MEK/ERK pathway is involved in the G1 arrest induced by p14ARF in p53-/-HCT cells. The results indicate that ERK1/2 and p21 were activated upon p14ARF induction. Totally, the functional roles of ERK and p21 for ARF in p53-independent tumor suppression were demonstrated.
引用
收藏
页码：415 / 422
页数：8
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