SLC25A10 promotes cisplatin resistance by inhibiting ferroptosis in cervical cancer

Background Cisplatin (DDP)-based chemotherapy remains the first-line treatment for cervical cancer (CC). However, patients with CC often develop primary or acquired resistance when treated with DDP, and thus the discovery of new therapeutic targets and combination therapy regimens are urgently needed to overcome DDP resistance. Methods The expression of SLC25A10 and its correlation with the clinicopathology of CC were analyzed using bioinformatics analysis and partial tissue analysis. The function and mechanism of SLC25A10 were investigated via a series of in vivo and in vitro experiments. Results SLC25A10 expression was significantly increased in human cervical cancer tissues according to TCGA data and clinical samples and was correlated with the clinicopathological characteristics of patients. Cell function experiments and in vivo xenograft tumor growth experiments showed that SLC25A10 promotes CC growth, migration and DDP resistance. Further studies on the molecular mechanism revealed that the inhibition of SLC25A10 expression restricted GSH transport, which induced intracellular lipid peroxidation and the accumulation of reactive oxygen species and promoted iron-mediated death in CC cells. Conclusion SLC25A10 may be a new therapeutic target to overcome cisplatin resistance and improve the efficacy of chemotherapy in CC. Keywords cervical cancer; SLC25A10; ferroptosis; cisplatin