Guseva Natalya V, Taghiyev Agshin F, Rokhlin Oskar W, Cohen Michael B
Department of Pathology, University of Iowa, Iowa City, Iowa 52242-1087, USA.
J Cell Biochem. 2004 Jan 1;91(1):70-99. doi: 10.1002/jcb.10707.
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.
前列腺癌死亡率源于转移，且常伴随着从雄激素依赖型生长向雄激素非依赖型生长的进展。不幸的是，目前尚无有效的治疗方法可提高转移性前列腺癌患者的生存率。缺乏有效治疗方法部分反映出对该疾病发生和进展所涉及分子机制的了解不足。细胞凋亡，即程序性细胞死亡，是一种细胞自杀机制，使多细胞生物体能够调节组织中的细胞数量。凋亡抑制似乎是促成前列腺癌发生和进展的关键病理生理因素。了解凋亡抑制机制可能是开发更有效治疗方法的基础。与其他恶性肿瘤，特别是造血系统肿瘤相比，我们对前列腺癌中细胞凋亡的了解相对有限。因此，仍迫切需要更好地了解这种恶性肿瘤中的细胞凋亡。在本综述中，我们重点关注了前列腺癌中已知的细胞凋亡情况，更具体地说，是作为潜在治疗靶点的受体/配体介导的凋亡途径。
