“…In lung adenocarcinoma, miR-296-3p also contributes to the inhibition of Ras, leading to the increased chemotherapy sensitivity [78]. It is also reported that miR-296-5p inhibited stemness potency and EMT via BRM/SWI2-related gene 1 and neuregulin 1, respectively [79]. Intriguingly, miR-95 knockdown could repress EMT and CSCs phenotype through dual frizzled class receptor 4, GATA3 GATA binding protein 3, GBM Glioblastoma, GC gastric cancer, HCPT hydroxycamptothecine, IGF1R insulin like growth factor 1 receptor, LC lung cancer, MK2 MAPK activated protein kinase 2, MRP5 multidrug resistant protein 5, NA not acquired, NIN1 Netrin 1, NPC Nasopharyngeal carcinoma, OC ovarian cancer, Oct4 Octamer-binding protein 4, ONECUT2 one cut homeobox 2, PC Pancreatic cancer, PRKCA Protein kinase C alpha, RAC1 Ras-related C3 botulinum toxin substrate 1, Rab6 Ras-related protein Rab-6a, RKIP Raf kinase inhibitory protein, SN38 7-ethyl-10-hydroxycamptothecin, SOX SRY-box transcription factor, TGM2 transglutaminase 2, TMZ temozolomide, TP53INP1 tumor protein P53 inducible nuclear protein 1, YAP1 Yes associated protein 1 specificity phosphatase 5-dependent MAPK pathway [80].…”