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MiR-155-5p inhibits PDK1 and promotes autophagy via the mTOR pathway in cervical cancer

Fang WangThe Second Hospital of Tianjin Medical University, 300211 Tianjin, ChinaShu ShanDepartment of Gynecology and Obstetrics, Affiliated Tongji Hospital, Tongji University, Shanghai, ChinaYan HuoThe Second Hospital of Tianjin Medical University, 300211 Tianjin, ChinaZipeng XieSchool of Basic Medical Sciences, Tianjin Medical University, 300070 Tianjin, ChinaYehong FangThe First Affiliated Hospital of Jinzhou Medical University, 121000 Shenyang, ChinaZhiying QiThe Second Hospital of Tianjin Medical University, 300211 Tianjin, ChinaFengzhen ChenThe Second Hospital of Tianjin Medical University, 300211 Tianjin, ChinaYongmei LiDepartment of Pathogen Biology, School of Basic Medical Sciences, Tianjin Medical University, 300070 Tianjin, China. Electronic address: [email protected]Bei SunKey Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Lab. of Metabolic Diseases, Tianjin Metabolic Diseases Hospital & Institute of Endocrinology, Tianjin Medical University, 300070 Tianjin, China. Electronic address: [email protected]

2018en

ABI

Annotatsiya

Cervical cancer is one of the most common malignant tumors and the leading cause of cancer-related mortality in women. Persistent cervical infection by high-risk human papillomavirus (hrHPV) is related to cervical cancer. MicroRNAs could regulate autophagy caused by viral infection. The aim of the present study was to investigate the regulation of autophagy by miR-155-5p in cervical cancer. In HPV+ human cervical lesion tissues, miR-155-5p expression was found to be markedly decreased. Compared to C33A cancer cells (HPV-), the miR-155-5p expression was significantly lower in Siha and HeLa cells (HPV+), which are both hrHPV positive. The level of autophagy was higher in C33A cells than in Siha and HeLa cells. In addition, in C33A, Siha and HeLa cervical cancer cells, miR-155-5p overexpression promoted autophagy, whereas miR-155-5p downregulation had the opposite effects. Furthermore, miR-155-5p downregulation suppressed LC3 and promoted P62 protein expression in C33A cells through promoting the PDK1/mTOR pathway, whereas miR-155-5p overexpression recovered LC3 and suppressed P62 protein expression by suppressing PDK1/mTOR signaling. Taken together, our results indicate the importance of miR-155-5p in cervical cancer cells and suggest a novel mechanism of hrHPV in promoting cervical lesions.

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Identifikatorlar

DOI: 10.1016/j.biocel.2018.04.005

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