(a) The mutation of EZH2 usually turns on gene transcription. (b) Overexpression of EZH2 in cancer trimethylates H3K27 to inhibit gene expression, especially among tumor suppressor genes. (c) Cyclin-dependent kinase 1/2 phophorylates EZH2 at Th350 which results in deregulating tumor suppressor genes by increasing H3K27-trimethylation levels at promoters of EZH2 targeted genes. (d) Proposed anti-tumor mechanisms of action of CDK1/2 and EZH2/Th350 inhibitors.
