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Fig. 4 | Journal of Hematology & Oncology

Fig. 4

From: Prognostic and therapeutic value of disruptor of telomeric silencing-1-like (DOT1L) expression in patients with ovarian cancer

Fig. 4

DOT1L regulates the transcription of G1 arrest genes CDK6 and CCND3 through H3K79 dimethylation. a Genomic distribution of DOT1L ChIP-seq peaks in SK-OV-3 cells. The proportion of DOT1L peaks was 8.60% distributed in promoters, 3.20% in exons, 39.60% in introns, and 48.6% in intergenics. b The average distribution of DOT1L-bound peaks near TSS. c and d RT-PCR detecting the change of primary G1 arrest genes, D-type cyclins (D1, D2, and D3), cyclin E, Cdks (2, 4, and 6) in mRNA levels in SK-OV-3 cells knocking down of DOT1L with shDOT1L shRNAs lentiviral particles (c) and DOT1L inhibitors, EPZ004777 and SGC0946 (d) (P < 0.05, Student’s t test, data represented as mean±SD). e and f DOT1L transcriptionally regulates the expression of CDK6 (e) and CCND3 (f) through induction of H3K79 dimethylation in the binding regions of these genes. Chromatin immunoprecipitation (ChIP) PCR assays were performed in a loss-of-function system. SK-OV-3 cells were transfected with shDOT1L shRNAs and shCON lentiviral particles and ChIP assays using anti-DOT1L and anti-H3K79me2 antibodies were performed with ChIP primers targeting the binding regions of CDK6 and CCND3 (P < 0.05, Student’s t test, data represented as mean±SD)

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