“…Tumor Supressor miRNAs Regulated Gene Expressions References miR-206 cMET, CCND1 and CDK6 [27] miR-214 EZH2, β-catenin [28,29] miR-223 STMN1 [30] miR-302b AKT2 [31] miR-339 ZNF689 [32] miR-15a, miR16 and miR-107 WNT3A [33] miR-375 YAP and AEG-1 [34] miR-424-5p TRIM 29 [35] miR-501-3p LIN7A [36] miR-874 DOR, EGFR and ERK [37] miR-140 MMP9 [38] Oncogenic miRNAs Regulated Gene Expressions and/or pathways miR-1914 PI3K/Akt [39] miR-660-5p PI3K/Akt [40] miR125a-5p PI3K/Akt [41] miR-3131 DTHD1 and XAF1 [42] miR-122 Induced HCV replication [43] miR-17-5p PTEN, GalNT7, Vimentin [44] miR-18a ESR1 [45] miR-32 PTEN [46] miR-92b SMAD7 [47] miR-93 PTEN, CDKN1A, c-Met/p13k/AKT pathway [48] miR-101 FOS oncogene [49] miR-106b EMT [50] miR-130b PPAR-γ, TP53INP1 [51] miR-155 c-Myc, C/EBPβ, APC, β-catenin, Cyclin D1, TP53INP1 [52] miR-197 Wnt/β-catenin, Axin-2, NKD1 and DKK2 [53] miR-219-5p Cadherin 1 [54] miR-221 and miR-222 PHF2, AKT pathway, PTEN, CDK inhibitor p27 and DDIT4 [55] Environmental factors, in addition to mutations, have an impact on the mTOR pathway activity. Under hypoxic conditions, HIF-2α was upregulated in steatotic HCC, resulting in activated PI3K and increased levels of phosphorylated AKT, GSK3B and mTOR [26].…”