14-3-3σ regulation by p53 mediates a chemotherapy response to 5-fluorouracil in MCF-7 breast cancer cells via Akt inactivation

被引：18
|
作者：
Zheng, Guopei [4 ]
Xiong, Yan [3 ]
Yi, Sisi [4 ]
Zhang, Weijia [4 ]
Peng, Bo [4 ]
Zhang, Qiong [1 ,2 ]
He, Zhimin [1 ,2 ,4 ]
机构：
[1] Guangzhou Med Univ, Canc Res Inst, Guangzhou 510095, Guangdong, Peoples R China
[2] Guangzhou Med Univ, Canc Hosp, Guangzhou 510095, Guangdong, Peoples R China
[3] Guangzhou Med Univ, Dept Pharmacol, Guangzhou 510095, Guangdong, Peoples R China
[4] Cent S Univ, Xiangya Sch Med, Canc Res Inst, Changsha 410078, Hunan, Peoples R China
来源：
FEBS LETTERS | 2012年 / 586卷 / 02期
基金：
中国国家自然科学基金;
关键词：
Breast cancer; Drug resistance; Methylation; 14-3-3; sigma; Akt; p53; SUPPRESSES TUMOR-GROWTH; FACTOR-KAPPA-B; DNA-DAMAGE; PROGRESSION; EXPRESSION; RESISTANCE; APOPTOSIS; PLAYS;
D O I：
10.1016/j.febslet.2011.11.034
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：
We previously demonstrated that 14-3-3 sigma was downregulated in 5-fluorouracil (5-Fu)-resistant MCF-7 breast cancer cells (MCF-7/5-Fu). Here, we found that stably enhanced 14-3-3 sigma expression strengthened the effects of 5-Fu, Mitoxantrone and cDDP. 14-3-3 sigma stabilised the p53 protein and bound Akt to inhibit its activity and its downstream targets: survivin, Bcl-2 and NF-kappa B-p50. In addition, decreased p53 expression, but not promoter hypermethylation, was responsible for the downregulation of 14-3-3 sigma in MCF-7/5-Fu cells. Meanwhile, initial treatments with high concentrations of 5-Fu clearly induced 14-3-3 sigma and p53 expression in a time-dependent manner. 14-3-3 sigma-mediated molecular events that synergise with p53 may play important roles in the chemotherapy of breast cancer. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码：163 / 168
页数：6
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