论文部分内容阅读
The roles of ClC-3 Cl channels in apoptosis induced by paclitaxel in nasopharyngeal carcinoma CNE2Z cells were studied by patch-clamp and molecular techniques, flow cytometry and atomic force microscopy.The anticancer drug paclitaxel activated a Cl-current and induced apoptosis in a concentration-dependent manner.The current was volume-sensitive, and was inhibited by Cl channel blockers.Paclitaxel treatment increased ClC3 expression significantly.Knockdown of ClC-3 expression by siRNA inhibited paclitaxel-induced Cl currents and apoptosis.