Death receptor-induced cell death in prostate cancer

被引:38
作者
Guseva, NV
Taghiyev, AF
Rokhlin, OW
Cohen, MB
机构
[1] Univ Iowa, Dept Pathol, Iowa City, IA 52242 USA
[2] Univ Iowa, Dept Urol, Iowa City, IA 52242 USA
[3] Univ Iowa, Dept Epidemiol, Iowa City, IA 52242 USA
关键词
apoptosis; death receptors; prostate cancer;
D O I
10.1002/jcb.10707
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
Prostate cancer mortality results from metastasis and is often coupled with progression from androgen-dependent to androgen-independent growth. Unfortunately, no effective treatment for metastatic Prostate cancer increasing patient survival is available. The absence of effective therapies reflects in part a lack of knowledge about the molecular mechanisms involved in the development and progression of this disease. Apoptosis, or programmed cell death, is a cell suicide mechanism that enables multicellular organisms to regulate cell number in tissues. Inhibition of apoptosis appears to be a critical pathophysiological factor contributing to the development and progression of prostate cancer. Understanding the mechanism(s) of apoptosis inhibition may be the basis for developing more effective therapeutic approaches. Our understanding of apoptosis in prostate cancer is relatively limited when compared to other malignancies, in particular, hematopoietic tumors. Thus, a clear need for a better understanding of apoptosis in this malignancy remains. In this review we have focused on what is known about apoptosis in prostate cancer and, more specifically, the receptor/ligand-mediated pathways of apoptosis as potential therapeutic targets. (C) 2003 Wiley-Liss, Inc.
引用
收藏
页码:70 / 99
页数:30
相关论文
共 222 条
[1]   Molecular genetics of prostate cancer [J].
Abate-Shen, C ;
Shen, MM .
GENES & DEVELOPMENT, 2000, 14 (19) :2410-2434
[2]   The Bcl-2 protein family: Arbiters of cell survival [J].
Adams, JM ;
Cory, S .
SCIENCE, 1998, 281 (5381) :1322-1326
[3]  
Amundson SA, 2000, CANCER RES, V60, P6101
[4]   Death receptors: Signaling and modulation [J].
Ashkenazi, A ;
Dixit, VM .
SCIENCE, 1998, 281 (5381) :1305-1308
[5]   Targeting death and decoy receptors of the tumour-necrosis factor superfamily [J].
Ashkenazi, A .
NATURE REVIEWS CANCER, 2002, 2 (06) :420-430
[6]   On the TRAIL to apoptosis [J].
Baetu, TM ;
Hiscott, J .
CYTOKINE & GROWTH FACTOR REVIEWS, 2002, 13 (03) :199-207
[7]   The NF-kappa B and I kappa B proteins: New discoveries and insights [J].
Baldwin, AS .
ANNUAL REVIEW OF IMMUNOLOGY, 1996, 14 :649-683
[8]   Control of oncogenesis and cancer therapy resistance by the transcription factor NF-κB [J].
Baldwin, AS .
JOURNAL OF CLINICAL INVESTIGATION, 2001, 107 (03) :241-246
[9]   Constitutive nuclear factor-κB-RelA activation is required for proliferation and survival of Hodgkin's disease tumor cells [J].
Bargou, RC ;
Emmerich, F ;
Krappmann, D ;
Bommert, K ;
Mapara, MY ;
Arnold, W ;
Royer, HD ;
Grinstein, E ;
Greiner, A ;
Scheidereit, C ;
Dörken, B .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 100 (12) :2961-2969
[10]   Control of apoptosis by Rel/NF-κB transcription factors [J].
Barkett, M ;
Gilmore, TD .
ONCOGENE, 1999, 18 (49) :6910-6924