Journal
PROSTATE
Volume 68, Issue 15, Pages 1615-1623Publisher
WILEY
DOI: 10.1002/pros.20828
Keywords
prostate cancer; apoptosis; BCL-2 family; ESR; UPR
Categories
Funding
- Edwin Beer Award
- NIH [R01 DK 53525-12]
- Markey Cancer Center
- University of Kentucky College of Medicine
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Molecular targeting of apoptotic signaling pathways has been extensively studied in recent years and directed towards the development of effective therapeutic modalities for treating advanced androgen-independent prostate tumors. The majority of therapeutic agents act through intrinsic or mitochondrial pathways to induce programmed cell death. The induction of apoptosis through endoplasmic reticulum (ER) stress pathways may provide an alternative to treat patients. The functional interaction between the BCL-2 family members and regulation of calcium homeostasis in the ER provides a critical link to the life or death outcome of the cell. Apoptosis induction mediated by ER stress-inducing agents is just beginning to be exploited for therapeutic targeting of prostate tumors. Insightful dissection of recently discovered apoptotic signaling pathways that function through the endoplasmic reticulum may identify novel molecules that could effectively target both androgen-dependent and androgen-independent prostate tumors. In this review, we focus on linking ER stress-induced apoptosis to therapeutic targeting of prostate tumors and dissect its cross-talk with the intrinsic and extrinsic apoptotic pathways. Prostate 68: 1615-1623, 2008. (C) 2008 Wiley-Liss, Inc.
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