TGFβ1 induces apoptosis in invasive prostate cancer and bladder cancer cells via Akt-independent, p38 MAPK and JNK/SAPK-mediated activation of caspases

被引：47
|
作者：
Al-Azayzih, Ahmad [1 ,2 ]
Gao, Fei [1 ,2 ]
Goc, Anna [1 ,2 ]
Somanath, Payaningal R. [1 ,2 ,3 ,4 ]
机构：
[1] Georgia Hlth Sci Univ, Coll Pharm, Univ Georgia, Augusta, GA 30912 USA
[2] Charlie Norwood VA Med Ctr, Augusta, GA USA
[3] Georgia Hlth Sci Univ, Dept Med, Augusta, GA USA
[4] Georgia Hlth Sci Univ, Vasc Biol Ctr, Augusta, GA USA
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2012年 / 427卷 / 01期
基金：
美国国家卫生研究院;
关键词：
Prostate cancer; TGF beta; Apoptosis; P38; MAPK; JNK; Akt; GROWTH-FACTOR-BETA; TGF-BETA; SIGNALING PATHWAYS; BREAST-CANCER; KINASE CASCADE; INHIBITION; TRANSFORMATION; RECEPTOR; PHOSPHORYLATION; ANGIOGENESIS;
D O I：
10.1016/j.bbrc.2012.09.035
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：
Recent findings indicate that advanced stage cancers shun the tumor suppressive actions of TGF beta and inexplicably utilize the cytokine as a tumor promoter. We investigated the effect of TGF beta 1 on the survival and proliferation of invasive prostate (PC3) and bladder (T24) cancer cells. Our study indicated that TGF beta 1 decreased cell viability and induced apoptosis in invasive human PC3 and 124 cells via activation of p38 MAPK-JNK-Caspase9/8/3 pathway. Surprisingly, no change in the phosphorylation of pro-survival Akt kinase was observed. We postulate that TGF beta 1 pathway may be utilized for specifically targeting urological cancers without inflicting side effects on normal tissues. (C) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码：165 / 170
页数：6
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