Ca2+ homeostasis in apoptotic resistance of prostate cancer cells

被引:72
|
作者
Prevarskaya, N
Skryma, R
Shuba, Y
机构
[1] USTL, Lab Physiol Cellulaire, INSERM, F-59655 Villeneuve Dascq, France
[2] NASU, Bogomolets Physiol Inst, UA-01024 Kiev 24, Ukraine
关键词
prostate cancer; apoptosis; calcium signaling; androgen-independency; endoplasmic reticulum; store-operated channels; Bcl-2;
D O I
10.1016/j.bbrc.2004.08.037
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
Ca2+ is a universal messenger regulating many physiological functions including such an important one, as the ability of the cell to undergo orderly self-destruction upon completion of its mission, called apoptosis. If this function is compromised unwanted cells may eventually take over the tissue turning it into a cancer. Ca2+ dependency of apoptosis, when its all aspects are learned and understood and key molecular players identified, may provide a good opportunity for controlling tumor growth. In the present mini-review we describe the major molecular determinants of Ca2+ homeostasis in prostate cancer cells and establish their role in the transformation to apoptosis-resistant cell phenotypes typical of advanced androgen-independent prostate cancer. We show that the hallmark of such transformation is the inhibition of apoptosis pathway associated with endoplasmic reticulum Ca2+ store depletion. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:1326 / 1335
页数:10
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