We previously reported that AQP-3 aquaglyceroporin and ClC-3 chloride channels could form complexes to regulate cell volume in nasopharyngeal carcinoma cells.
Our data demonstrated that the selective antitumor activities of DHA in NPC may occur through the specific activation of the CLC-3 Cl<sup>-</sup> channel, leading to Cl<sup>-</sup> efflux, and induced AVD, then led to [Ca<sup>2+</sup> ]<sub>i</sub> accumulation and caspase-3 activation, and finally induced apoptosis.
Nevertheless, ClC-3 knockdown had little effect on ROS levels, indicating that ROS acted upstream of ClC-3 and that both ROS and ClC-3 participated in EBSS-induced autophagy regulation in CNE-2Z.
Here, we showed that the involvement of ClC-3 chloride channel in the selective cytotoxicity of DSF/Cu<sup>2+</sup> in the poorly-differentiated nasopharyngeal carcinoma.