RETRACTED: Down-Regulation of Notch-1 Is Associated With Akt and FoxM1 in Inducing Cell Growth Inhibition and Apoptosis in Prostate Cancer Cells (Retracted article. See vol. 117, pg. 1962, 2016)

被引:74
|
作者
Wang, Zhiwei [1 ]
Li, Yiwei
Ahmad, Aamir
Banerjee, Sanjeev
Azmi, Asfar S.
Kong, Dejuan
Wojewoda, Christine
Miele, Lucio [2 ]
Sarkar, Fazlul H. [1 ]
机构
[1] Wayne State Univ, Sch Med, Dept Pathol, Karmanos Canc Inst, Detroit, MI 48201 USA
[2] Univ Mississippi, Inst Canc, Jackson, MS 39216 USA
关键词
NOTCH-1; PROSTATE CANCER; CELL GROWTH; APOPTOSIS; Akt; FoxM1; FACTOR-KAPPA-B; M1 TRANSCRIPTION FACTOR; VIVO MOLECULAR EVIDENCE; IN-VITRO; SIGNALING PATHWAY; GENISTEIN; TARGET; INACTIVATION; COMBINATION; DOCETAXEL;
D O I
10.1002/jcb.22770
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
Although many studies have been done to uncover the mechanisms by which down-regulation of Notch-1 exerts its anti-tumor activity against a variety of human malignancies, the precise molecular mechanisms remain unclear. In the present study, we investigated the cellular consequence of Notch-1 down-regulation and also assessed the molecular consequence of Notch-1-mediated alterations of its downstream targets on cell viability and apoptosis in prostate cancer (PCa) cells. We found that the down-regulation of Notch-1 led to the inhibition of cell growth and induction of apoptosis, which was mechanistically linked with down-regulation of Akt and FoxM1, suggesting for the first time that Akt and FoxM1 are downstream targets of Notch-1 signaling. Moreover, we found that a "natural agent" (genistein) originally discovered from soybean could cause significant reduction in cell viability and induced apoptosis of PCa cells, which was consistent with down-regulation of Notch-1, Akt, and FoxM1. These results suggest that down-regulation of Notch-1 by novel agents could become a newer approach for the prevention of tumor progression and/or treatment, which is likely to be mediated via inactivation of Akt and FoxM1 signaling pathways in PCa. J. Cell. Biochem. 112: 78-88, 2011. (C) 2010 Wiley-Liss, Inc.
引用
收藏
页码:78 / 88
页数:11
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