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Journal articles
Down-regulation of DcR2 sensitizes androgen-dependent prostate cancer LNCaP cells to TRAIL-induced apoptosis.
Abstract : UNLABELLED: ABSTRACT: BACKGROUND: Dysregulation of many apoptotic related genes and androgens are critical in the development, progression, and treatment of prostate cancer. The differential sensitivity of tumour cells to TRAIL-induced apoptosis can be mediated by the modulation of surface TRAIL receptor expression related to androgen concentration. Our previous results led to the hypothesis that downregulation of TRAIL-decoy receptor DcR2 expression following androgen deprivation would leave hormone sensitive normal prostate cells vulnerable to the cell death signal generated by TRAIL via its pro-apoptotic receptors. We tested this hypothesis under pathological conditions by exploring the regulation of TRAIL-induced apoptosis related to their death and decoy receptor expression, as also to hormonal concentrations in androgen-sensitive human prostate cancer, LNCaP, cells. RESULTS: In contrast to androgen-insensitive PC3 cells, decoy (DcR2) and death (DR5) receptor protein expression was correlated with hormone concentrations and TRAIL-induced apoptosis in LNCaP cells. Silencing of androgen-sensitive DcR2 protein expression by siRNA led to a significant increase in TRAIL-mediated apoptosis related to androgen concentration in LNCaP cells. CONCLUSIONS: The data support the hypothesis that hormone modulation of DcR2 expression regulates TRAIL-induced apoptosis in LNCaP cells, giving insight into cell death induction in apoptosis-resistant hormone-sensitive tumour cells from prostate cancer. TRAIL action and DcR2 expression modulation are potentially of clinical value in advanced tumour treatment.
Cited literature [50 references]
https://www.hal.inserm.fr/inserm-00674028
Contributor : Ed. Bmc <>
Submitted on : Friday, February 24, 2012 - 5:06:56 PM
Last modification on : Friday, June 18, 2021 - 4:06:07 PM
Long-term archiving on: : Friday, November 23, 2012 - 2:45:55 PM
Contributor : Ed. Bmc <>
Submitted on : Friday, February 24, 2012 - 5:06:56 PM
Last modification on : Friday, June 18, 2021 - 4:06:07 PM
Long-term archiving on: : Friday, November 23, 2012 - 2:45:55 PM