Fig. 3

RASA1 was the direct target of miR-182 and the inhibition of RASA1 promoted angiogenesis. a miR-182 and its predicted binding sequence in the 3’UTR of RASA1. The mutant sequence was constructed by changing their complementary sites. b The SK-HEP-1 cells were co-transfected with miR-182 mimics or inhibitors or NC and 100 ng firefly luciferase reporter plasmid containing wild-type or mutant type 3’UTR of RASA1. After incubation for 48 h, the firefly luciferase activity of each sample was detected and normalized to the renilla luciferase activity. The data represent the mean ± SEM of triplicates. c The protein levels of RASA1 were examined by western blot after transfected with miR-182 mimics or inhibitors. d IHC assays were applied to explore the protein levels of RASA1 in 36 HCC tissues. The representative images were shown at the 400× magnification. The medium level of all 36 cases was chosen as the cut-off point for separating low-miR-182 (n = 18) and high-miR-182 (n = 18) groups. e Capillary tube formation assays was used to detect the angiogenesis effects of RASA1 suppression. The data represent the mean ± SEM of triplicates. (*P < 0.05, **P < 0.01)