Reduced response of prostate cancer cells to TRAIL is modulated by NFκB-mediated inhibition of caspases and Bid activation
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- Published online on: July 1, 2002 https://doi.org/10.3892/ijo.21.1.111
- Pages: 111-117
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Abstract
We describe the effects of tumor necrosis factor α-related apoptosis inducing ligand (TRAIL) on the induction of apoptosis in two related prostate cancer cell lines, PC3AR and PC3Neo. TRAIL is a potent drug, which induces apoptosis preferentially in cancer cells. Treatment of prostate cancer cells, reduced survival by ~41% in PC3AR, but only ~18% PC3Neo were killed. Western analysis demonstrated that increased apoptotic response of PC3AR cells may be due to differential response of death receptors DR4, DR5 and decoy receptors DcR1 and DcR2. Caspases-8, -9, -3 and Bid were highly activated in PC3AR cells compared to PC3Neo. Furthermore, lower apoptotic response of PC3Neo was probably due to higher expression of NFκB. Blocking the function of NFκB by adenoviral infection of mutated IκB, increased apoptotic response confirming the influence of NFκB. Thus, we have demonstrated the role of NFκB in the differential response of prostate cancer cells to TRAIL.
