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.
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.
We previously reported that AQP-3 aquaglyceroporin and ClC-3 chloride channels could form complexes to regulate cell volume in nasopharyngeal carcinoma cells.