Skip to main content
Fig. 7 | Clinical Epigenetics

Fig. 7

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

Fig. 7

DOT1L silencing or inhibition demethylates H3K79 and suppresses transcription of c-Myc. a The Pearson correlation between DOT1L and c-Myc expression in patients with colorectal cancer in the TCGA COAd datasheet from the GEPIA. b Relative mRNA expression of c-Myc in patients with colorectal cancer in the TCGA COAd datasheet from the GEPIA. c Protein expression of c-Myc in SW480 and HCT116 cells after DOT1L knockdown or inhibition. Gray ratio of each blot was analyzed by using the ImageJ software and protein/GAPDH ratio was shown. d mRNA expression of c-Myc, CDK2, Cyclin A2 in SW480, and HCT116 cells after DOT1L knockdown or inhibition. e H3K9 methylation (m1/2/3) was detected by using Western blot in SW480 and HCT116 cells after DOT1L knockdown or inhibition. Gray ratio of each blot was analyzed by using the ImageJ software and protein/H3 ratio was shown. f–h ChIP assay was performed to detect the binding region of H3K79me2 on the promoter of c-Myc in SW480 and HCT116 cells after DOT1L knockdown or inhibition. i, j IHC staining of c-Myc and H3K79me1/2/3 in xenografts obtained from subcutaneous injecting SW480 and HCT116 cells after DOT1L knockdown or inhibition within mice. Signal-positive rate was analyzed by using the IHC profiler in the ImageJ software

Back to article page