Combination therapy induces unfolded protein response and cytoskeletal rearrangement leading to mitochondrial apoptosis in prostate cancer

Development of therapeutic resistance is responsible for most prostate cancer (PCa) related mortality. Resistance has been attributed to an acquired or selected cancer stem cell phenotype. Here we report the histone deacetylase inhibitor apicidin (APC) or ER stressor thapsigargin (TG) potentiate paclitaxel (TXL)-induced apoptosis in PCa cells and limit accumulation of cancer stem cells. TXL-induced responses were modulated in the presence of TG with increased accumulation of cells at G1-phase, rearrangement of the cytoskeleton, and changes in cytokine release.

Source: Molecular Oncology - March 30, 2016 Category: Cancer & Oncology Authors: Sandeep Kumar, Ajay K. Chaudhary, Rahul Kumar, Jordan O'Malley, Anna Dubrovska, Xinjiang Wang, Neelu Yadav, David W. Goodrich, Dhyan Chandra Source Type: research