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MicroRNA26a inhibits cisplatin‐induced renal tubular epithelial cells apoptosis through suppressing the expression of transient receptor potential channel 6 mediated dynamin‐related protein 1

Acute kidney injury (AKI) is a common adverse reaction of the anticancer drug. Among these chemotherapeutic agents, cisplatin, an effective chemotherapeutic drug, is extensively applied to the treatment of solid tumours, yet various adverse reactions, especially AKI, often limit their use. However, the pathogenesis of AKI caused by cisplatin remains poorly clarified. Therefore, we tested whether microRNAs, which have been certified as key regulators of disease are involved in this process. AKI mouse and HK2 cells were treated with cisplatin. Annexin V/PI staining and cleaved caspase‐3 were used to assess apoptosis. Western blot analyses and qRT‐PCR were used to evaluate the protein and mRNA level of TRPC6 and DRP1. miR‐26a was remarkably decreased in cisplatin‐induced AKI and in cisplatin co‐cultured HK2 cells. Furthermore, we used a miR‐26a mimics in vitro and found that apoptosis was alleviated than that in the control cells. We further verified that miR‐26a protected against cisplatin‐induced cell apoptosis by acting on transient receptor potential channel 6 (TRPC6) which can regulate the expression of dynamin‐related protein 1 (DRP1), thus inhibited the mitochondrial apoptosis pathway. Therefore, the study unveiled that miR‐26a/TRPC6/DRP1 is a novel protective pathway in cisplatin‐induced AKI and may be targeted for the prevention and treatment of drug‐related renal injury.