The oxidoreductase CLIC4 is required to maintain mitochondrial function and resistance to exogenous oxidants in breast cancer cells
Heba Al Khamici, Vanesa C. Sanchez, Hualong Yan, Christophe Cataisson, Aleksandra M. Michalowski, Howard H. Yang, Luowei Li, Maxwell P. Lee, Jing Huang, Stuart H. Yuspa
Abstract
-treated control and CLIC4-null cells revealed upregulation of genes associated with ROS-induced apoptosis and downregulation of genes that sustain mitochondrial functions. Accordingly, tumors that formed from transplantation of CLIC4-deficient 6DT1 cells were highly necrotic. These results highlight a critical role for CLIC4 in maintaining redox-homeostasis and mitochondrial functions in 6DT1 cells. Our findings also raise the possibility of targeting CLIC4 to increase cancer cell sensitivity to chemotherapeutic drugs that are based on elevating ROS in cancer cells.
Topics & Concepts
Cell biologyMitochondrionBiologyDownregulation and upregulationCancer cellApoptosisMitochondrial ROSMolecular biologyReactive oxygen speciesBiochemistryCancerGeneGeneticsMitochondrial Function and PathologyIon channel regulation and functionATP Synthase and ATPases Research