Huang Fengyu, Wang Peitao, Wang Xinsheng
Department of Clinical Medicine, Medical College of Qingdao University, Qingdao, Shandong 266021, P.R. China.
Department of Urology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266011, P.R. China.
Oncol Lett. 2018 Aug;16(2):1975-1980. doi: 10.3892/ol.2018.8833. Epub 2018 May 30.
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.
普遍认为内质网应激可能迅速诱导细胞凋亡。本研究的目的是探讨毒胡萝卜素对前列腺癌细胞凋亡诱导的影响，并探究其可能的机制。选用细胞计数试剂盒-8来测定毒胡萝卜素（0、1、10和100 nM）对PC3细胞增殖的影响。用毒胡萝卜素处理可有效抑制前列腺癌细胞的增殖，且毒胡萝卜素显著提高前列腺癌细胞的凋亡率和半胱天冬酶-3/9活性。在前列腺癌细胞中，用毒胡萝卜素处理后，磷酸化（p）-RAC-α丝氨酸苏氨酸蛋白激酶、p-雷帕霉素作用靶点、F-肌动蛋白和桩蛋白的蛋白表达显著降低，而丝切蛋白-1蛋白表达显著增加。总体而言，本研究数据表明毒胡萝卜素通过丝切蛋白-1和桩蛋白诱导前列腺癌细胞凋亡。
