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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: RBM38 plays a tumor-suppressor role via stabilizing the p53-mdm2 loop function in hepatocellular carcinoma

Fig. 3

RBM38 suppressed anchorage dependent growth of human liver cancer cells. a The growth of cells over 6 days was measured using cell counting kit (CCK-8) assays. RBM38 indicates RBM38 overexpressing SMMC7721 and HepG2 cells; NC indicates SMMC7721 and HepG2 cells transfected with a vector-expressing GFP. The proliferation rate of SMMC7721-RBM38-OE and HepG2-RBM38-OE was significantly decreased compared with control cells, respectively. Data were mean values of three separate experiments mean ± SEM. b The growth of cells over 15 days was measured using colony formation assays. Clone formation of RBM38 overexpression arbitrarily set at 100% in control cells (NC). The colony numbers of SMMC7721-RBM38-OE and HepG2-RBM38-OE were significantly reduced and the colony sizes were significantly shrunk compared to control cells, respectively. Representative photographs and quantification are shown. Data were mean values of three separate experiments mean ± SEM. c,d RT-PCR and Western blotting analysis of mdm2 overexpression in RBM38-OE cells. e The growth of cells over 6 days was measured using cell counting kit (CCK-8) assays. The proliferation rates of SMMC7721-RBM38-OE-MDM2-OE and HepG2-RBM38-OE-MDM2-OE were significantly increased compared with control cells, respectively. Data were mean values of three separate experiments mean ± SEM. f The growth of cells over 15 days was measured using colony formation assays. The colony numbers of SMMC7721-RBM38-OE-MDM2-OE and HepG2-RBM38-OE-MDM2-OE were significantly rescued and the colony sizes were significantly larger compared to control cells, respectively. Representative photographs and quantification are shown. Data were mean values of three separate experiments mean ± SEM

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