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- W2485812469 abstract "The insulin-like growth factor (IGF)-axis has been paradigmatically involved in hepatocellular carcinoma (HCC) tumor initiation, progression and drug resistance. Consequently, members of the IGF‑axis and most importantly, IGF-1 receptor (IGF-1R) have been considered as intriguing targets for HCC therapy. Few miRNAs have been recently reported to be associated with IGF‑1R regulation. The present study aimed to investigate the role of microRNA (miRNA/miR)‑486‑5p in the regulation of IGF‑1R and its downstream signaling cascades. miR‑486‑5p was markedly downregulated in hepatitis C virus‑induced HCC tissues and Huh‑7 cells. Forcing the expression of miR‑486‑5p in Huh‑7 cells resulted in the repression of IGF‑1R, mammalian target of rapamycin (mTOR), signal transducer and activator of transcription 3 (STAT3) and c‑Myc mRNA levels. Ectopic expression of miR‑486‑5p in Huh‑7 cells markedly repressed cellular viability, proliferation, migration and clonogenicity in a similar pattern to IGF‑1R small interfering RNAs, and were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, BrdU incorporation, wound healing and colony forming assays, respectively. Overall, the study findings demonstrated that miR‑486‑5p acts as a tumor suppressor in HCC through the repression of essential members of the IGF‑axis, including IGF‑1R and its downstream mediators mTOR, STAT3 and c‑Myc." @default.
- W2485812469 created "2016-08-23" @default.
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- W2485812469 date "2016-07-27" @default.
- W2485812469 modified "2023-10-02" @default.
- W2485812469 title "MicroRNA-486-5p enhances hepatocellular carcinoma tumor suppression through repression of IGF-1R and its downstream mTOR, STAT3 and c-Myc" @default.
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- W2485812469 doi "https://doi.org/10.3892/ol.2016.4914" @default.
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