Abstract
It is widely considered that endoplasmic reticulum stress may rapidly induce apoptosis. The aim of the present study was to investigate the effect of thapsigargin on the induction of apoptosis in prostate cancer cells, and to explore its possible mechanism. A Cell Counting Kit-8 was selected to determine the effect of thapsigargin (0, 1, 10 and 100 nM) on the proliferation of PC3 cells. Cell proliferation of the prostate cancer cells was effectively inhibited by treatment with thapsigargin, and thapsigargin significantly increased the rate of apoptosis and caspase-3/9 activities in prostate cancer cells. The protein expression of phosphorylated (p)-RAC-α serine threonine-protein kinase, p-mechanistic target of rapamycin, F-actin and paxillin were significantly decreased, and cofilin-1 protein expression was significantly increased by treatment with thapsigargin in prostate cancer cells. Overall, the data of the present study revealed that thapsigargin induced apoptosis in prostate cancer cells through cofilin-1 and paxillin.