miR-3188 regulates nasopharyngeal carcinoma proliferation and chemosensitivity through a FOXO1-modulated positive feedback loop with mTOR–p-PI3K/AKT-c-JUN

Mengyang Zhao, Rongcheng Luo, Yiyi Liu, Linyuan Gao, Zhaojian Fu, Qiaofen Fu, Xiaojun Luo, Yiyu Chen, Xiaojie Deng, Zixi Liang, Xin Li, Chao Cheng, Zhen Liu () and Weiyi Fang ()
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Mengyang Zhao: Cancer Center, Traditional Chinese Medicine-Integrated Hospital, Southern Medical University
Rongcheng Luo: Cancer Center, Traditional Chinese Medicine-Integrated Hospital, Southern Medical University
Yiyi Liu: Cancer Research Institute, Southern Medical University
Linyuan Gao: Cancer Research Institute, Southern Medical University
Zhaojian Fu: Cancer Research Institute, Southern Medical University
Qiaofen Fu: Cancer Research Institute, Southern Medical University
Xiaojun Luo: Cancer Center, Traditional Chinese Medicine-Integrated Hospital, Southern Medical University
Yiyu Chen: Cancer Research Institute, Southern Medical University
Xiaojie Deng: Cancer Research Institute, Southern Medical University
Zixi Liang: Cancer Research Institute, Southern Medical University
Xin Li: Cancer Research Institute, Southern Medical University
Chao Cheng: Cancer Research Institute, Southern Medical University
Zhen Liu: Cancer Research Institute, Southern Medical University
Weiyi Fang: Cancer Center, Traditional Chinese Medicine-Integrated Hospital, Southern Medical University

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract The biological role of miR-3188 has not yet been reported in the context of cancer. In this study, we observe that miR-3188 not only reduces cell-cycle transition and proliferation, but also significantly prolongs the survival time of tumour-bearing mice as well as sensitizes cells to 5-FU. Mechanistic analyses indicate that miR-3188 directly targets mTOR to inactivate p-PI3K/p-AKT/c-JUN and induces its own expression. This feedback loop further suppresses cell-cycle signalling through the p-PI3K/p-AKT/p-mTOR pathway. Interestingly, we also observe that miR-3188 direct targeting of mTOR is mediated by FOXO1 suppression of p-PI3K/p-AKT/c-JUN signalling. In clinical samples, reduced miR-3188 is an unfavourable factor and negatively correlates with mTOR and c-JUN levels but positively correlates with FOXO1 expression. Our studies demonstrate that as a tumour suppressor, miR-3188 directly targets mTOR to stimulate its own expression and participates in FOXO1-mediated repression of cell growth, tumorigenesis and NPC chemotherapy resistance.

Date: 2016
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DOI: 10.1038/ncomms11309

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