Drug interactions between the proteasome inhibitor bortezomib and cytotoxic chemotherapy, tumor necrosis factor (TNF) alpha, and TNF-related apoptosis-inducing ligand in prostate cancer.
作者： Arie Belldegrun , Matthew B Rettig , Yi-Ping Sun , Jiabin An , Myrna Fisher
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摘要: Purpose: Proteasome inhibition has been shown to be an effective anticancer therapy in many tumor models, including prostate cancer. We sought identify drug interactions between the proteasome inhibitor bortezomib and other apoptotic stimuli, cytotoxic chemotherapy necrosis factor-related apoptosis-inducing ligand (TRAIL). In addition, we wanted gain insight into role of nuclear factor κB as a mediator effects. Experimental Design: Prostate cancer cell lines (LNCaP, LAPC4, CL1, DU145) were treated with stimuli (TRAIL, chemotherapy, α), alone or combination. Apoptosis viability measured, median effect/combination index analyses used quantitate interactions. Nuclear activity at baseline response treatment was determined by gel shift reporter gene assays. Results: Bortezomib induced death androgen-dependent (LNCaP LAPC4) androgen-independent (CL1 lines, although cells more sensitive inhibition. synergized TRAIL α induce both cells. Conclusions: represent synergistic combination that warrants further evaluation vivo models
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