Fig. 5

HOXA3 functioned as a target of miR-10b, which suppressed proliferation, invasion and apoptosis of ccRCC cells. a Predicted duplex formation between human HOXA3 3’UTR and miR-10b. b The relative levels of miR-10 in ccRCC cells transfected with miR-10b mimic and miR-10b inhibitor, as determined by qRT-PCR. RNU44 was used as endogenous control. c Luciferase activity of wild-type (UTR-wt) or mutant (UTR-mut). HOXA3 3’UTR reporter gene in 786-O cells infected with the miR-10b mimic or negative control (NC) mimic. d qRT-PCR of HOXA3 in 786-O cells infected with shHOXA3, miR-10b mimic, miR-10b inhibitor or vector. e Western blot of HOXA3 in 786-O cells infected with shHOXA3, miR-10b mimic, miR-10b inhibitor or vector. f Cell viability of 786-O and A498 cells transfected with negative control (NC), shHOXA3, shHOXA3 + miR-10b mimic or shHOXA3 + miR-10b inhibitor for 48 h, as determined by MTT assay. g Invasion of ccRCC cells transfected with negative control (NC), shHOXA3, shHOXA3+ miR-10b mimic or shHOXA3 + miR-10b inhibitor, as gauged by transwell invasion assay. h Apoptosis of ccRCC cells transfected with negative control (NC), shHOXA3, shHOXA3+ miR-10b mimic or shHOXA3 + miR-10b inhibitor. *P < 0.05, **P < 0.01, compared to cells treated with control