miR‐138‐5p targets MCU to inhibit mitochondrial biogenesis and colorectal cancer growth

Abstract

AbstractmiR‐138‐5p has been identified as a novel cancer‐related miRNA molecule in a variety of malignancies. However, the functions and mechanisms underlying miR‐138‐5p in colorectal carcinoma (CRC) remains largely unknown. In the present study, we analysed the biological effects and clinical significance of miR‐138‐5p in CRC. miR‐138‐5p expression was analysed by quantitative real‐time PCR in CRC tissues and cell lines. The effects of miR‐138‐5p on CRC cell growth was detected by cell proliferation, colony formation, cell cycle and cell apoptosis assays in vitro and in vivo. Our data showed that miR‐138‐5p was significantly downregulated in CRC. Downregulated miR‐138‐5p was related with poor prognosis in patients with CRC. miR‐138‐5p suppressed CRC growth but promoted cell death both in vitro and in vivo. Online predictions and integrated experiments identified that miR‐138‐5p targeted MCU, and downregulated miR‐138‐5p promoted mitochondrial biogenesis in CRC. In the light of the underlying mechanisms, our results indicated that downregulated miR‐138‐5p led to increased expression of MCU, which subsequently increased the production of ROS to promote CRC growth. Our results indicated that downregulated miR‐138‐5p strengthened mitochondrial biogenesis through targeting MCU, thus contributing to CRC cell growth, which may provide a potential therapeutic target for CRC.