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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: CRISPR/Cas9-mediated knockout of NSD1 suppresses the hepatocellular carcinoma development via the NSD1/H3/Wnt10b signaling pathway

Fig. 2

NSD1 knockout inhibits cell proliferation, migration and invasion abilities in HCC. a, Expression of NSD1 in human immortalized liver cell line (HL-7702) and HCC cell lines (Huh7, Hep3B, SMMC-7721, HepG2, and SK-Hep1) determined by RT-qPCR and Western blot analysis. b, mRNA and protein expression following NSD1 overexpression in HepG2 cell line examined by RT-qPCR and Western blot analysis. c, Proliferation ability of HepG2 cells after overexpression of NSD1 determined by CCK-8 method and monoclonal formation assay. d, Migration and invasion ability of HepG2 cells following NSD1 overexpression determined by Transwell assay (× 100). e, Expression of NSD1 normalized to GAPDH in SK-Hep1 cells after knockout of NSD1 by CRISPR-Cas9 examined by Western blot analysis. f, Proliferation ability of SK-Hep1 cells after knockout of NSD1 measured by CCK-8 method and monoclonal formation assay. g, Migration and invasion ability of SK-Hep1 cells after knockout of NSD1 detected by Transwell assay (× 100). * p < 0.05 vs. the HL-7702 cell line, or the blank group (HepG2/SK-Hep1 cells without any treatment). Data (mean ± s.d.) among multiple groups were analyzed by one-way ANOVA, followed by Tukey’s post-hoc test, while those at different time points were analyzed by repeated measures ANOVA, followed by the Bonferroni’s post-hoc test. The experiment was repeated 3 times independently

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