Study reveals DCAF1 protein's role in colon cancer development through EZH2 phosphorylation DCAF1 EZH2 coloncancer epigenetics genesilencing oncogenes cancer histones H3K27me3 preclinical organoidmodels xenograftmodels USC NatureComms
By Dr. Priyom Bose, Ph.D.Apr 18 2023Reviewed by Benedette Cuffari, M.Sc. Initially, the DDB1 and CUL4 Associated Factor 1 was identified as a protein that interacts with human immunodeficiency virus 1 virion-associated protein and regulates cell cycles and cell proliferation.
The transrepression potential of DCAF1 in cancer cells can be eliminated through kinase-dead mutations. Thus, an H2AT120p-dependent mechanism is associated with DCAF1 function in maintaining inactive chromatin states and triggering oncogenic transformation. Enhancer of Zeste Homolog 2 is a highly conserved histone lysine methyltransferase that triggers the trimethylation of nucleosomal histone H3 at lysine 27 . EZH2 has been found overexpressed or mutated in many types of cancer and appears to be involved in tumor initiation and progression with poor clinical prognosis. Several studies have reported that the enzymatic activity of EZH2 is regulated by many posttranslational modifications, including phosphorylation.
About the study A recent Nature Communications study reveals that DCAF1 is overexpressed and phosphorylates EZH2 in colon cancer cells. Identification of the association between DCAF1 and non-histone modifications could provide better insights into oncogenic signaling pathways. This knowledge would enable the development of more effective strategies to treat colon and other types of cancer.
DCAF1-mediated EZH2T367p modulates the strength and nature of how EZH2 interacts with other components of the polycomb repressive complex 2 complex. Ultimately, EZH2 enhances the stability and histone methyltransferase activity toward H3K27. Notably, T367p was found to be an extremely important factor for EZH2 stability, which allows the effective regulation of EZH2 protein levels.
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