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• W2337353755 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." @default.
• W2337353755 created "2016-06-24" @default.
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• W2337353755 date "2016-04-20" @default.
• W2337353755 modified "2023-10-17" @default.
• W2337353755 title "miR-3188 regulates nasopharyngeal carcinoma proliferation and chemosensitivity through a FOXO1-modulated positive feedback loop with mTOR–p-PI3K/AKT-c-JUN" @default.
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• W2337353755 doi "https://doi.org/10.1038/ncomms11309" @default.
• W2337353755 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4842991" @default.
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• W2337353755 hasPublicationYear "2016" @default.
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