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Fig. 8 | Clinical Epigenetics

Fig. 8

From: Silencing or inhibition of H3K79 methyltransferase DOT1L induces cell cycle arrest by epigenetically modulating c-Myc expression in colorectal cancer

Fig. 8

Restoration of c-Myc partly rescued cell proliferation inhibition and cell cycle arrest induced by DOT1L silencing or inhibition in vitro and in vivo. a Cell growth curve was determined by using MTT assay in SW480 and HCT116 cells after DOT1L knockdown and c-Myc restoration. Vector control for c-Myc overexpression was used in both shGFP and shDOT1L-2 groups (similarly hereinafter). b BrdU assay was performed in SW480 and HCT116 cells after DOT1L knockdown and c-Myc restoration. c Soft agar assay was performed in SW480 and HCT116 cells after DOT1L knockdown and c-Myc restoration. d Cell cycle was detected by using flow cytometry in SW480 and HCT116 cells after DOT1L knockdown and c-Myc restoration. e Protein expression of cell cycle–related proteins including p21, p27, CDK2, Cyclin A2, and PCNA was detected by using Western blot in SW480 and HCT116 cells after DOT1L knockdown and c-Myc restoration. Gray ratio of each blot was analyzed by using the Image J software and protein/GAPDH ratio was shown. f, g The effect of c-Myc restoration on tumorigenicity of SW480 and HCT116 cells after DOT1L knockdown. Tumor volume, tumor weight, and H&E staining were performed to determine the capacity of tumorigenicity

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