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miR-138-5p targets MCU to inhibit mitochondrial biogenesis and colorectal cancer growth |
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| Authors: | Jianjun Zhu Chunle Zhang Zhengjie Wang Lihong Shi Li Li Hao Wu Ming Liu |
| Institution: | 1. Department of Medical Cellular Biology and Genetics, Shanxi Medical University, Taiyuan, China;2. Department of Nephrology, Kidney Research Institute, West China Hospital of Sichuan University, Chengdu, China;3. Department of Nuclear Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
Contribution: ?Investigation (supporting), Methodology (supporting), Software (supporting), Validation (supporting);4. Department of Human Anatomy, Shanxi Medical University, Taiyuan, China Contribution: ?Investigation (supporting), Methodology (supporting), Software (supporting), Validation (supporting), Visualization (supporting);5. Department of Medical Cellular Biology and Genetics, Shanxi Medical University, Taiyuan, China Contribution: Data curation (supporting), Formal analysis (supporting), ?Investigation (supporting), Methodology (supporting), Project administration (equal), Software (supporting), Supervision (equal), Validation (supporting) |
| Abstract: | miR-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. |
| Keywords: | colorectal carcinoma MCU miR-138-5p ROS tumour growth |