CLC3 regulates V-ATPase to enhance lysosomal degradation and cisplatin resistance in cervical cancer cells.

ABSTRACT: Chemoresistance remains a major challenge in cervical cancer (CVC) treatment. Lysosomal function, mediated by V-ATPase, is critical in cancer progression and drug resistance. CLC3, a chloride channel that regulates lysosomal acidification, may contribute to chemoresistance by modulating V-ATPase activity. This study aims to investigate the role of CLC3 in modulating lysosomal function, chemoresistance, and tumorigenesis in CVC. CLC3 expression in CVC cell lines was assessed, and chemoresistance was evaluated using IC50 calculations for cisplatin, paclitaxel, and 5-FU. Effects of CLC3 downregulation or overexpression on lysosomal pH, autophagy, apoptosis, cell proliferation, cell cycle progression, and tumor stemness were analyzed. A general V-ATPase inhibitor was used to assess changes in

SUBMITTER: Chen C 

PROVIDER: S-EPMC12783824 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature