Mutations and deletions of PRC2 in prostate cancer. (22nd March 2016)

• Record Type: Journal Article
• Authors: Jain, Payal; Di Croce, Luciano
• Is Part Of: BioEssays. Volume 38:Number 5(2016:May)
• Page Start: 446
• Page End: 454
• Publication Date: 2016-03-22
• Subjects: cancer -- epigenetic modifications -- Polycomb proteins -- PRC2; Molecular biology -- Periodicals; Cytology -- Periodicals; Developmental biology -- Periodicals; 572.8
• DOI: 10.1002/bies.201500162
• Languages: English
• ISSNs: 0265-9247

Abstract

Abstract : The Polycomb group of proteins (PcGs) are transcriptional repressor complexes that regulate important biological processes and play critical roles in cancer. Mutating or deleting EZH2 can have both oncogenic and tumor suppressive functions by increasing or decreasing H3K27me3. In contrast, mutations of SUZ12 and EED are reported to have tumor suppressive functions. EZH2 is overexpressed in many cancers, including prostate cancer, which can lead to silencing of tumor suppressors, genes regulating epithelial to mesenchymal transition (EMT), and interferon signaling. In some cases, EZH2 overexpression also leads to its use of non‐histone substrates. Lastly, PRC2 associated factors can influence the progression of cancer through progressive mutations or by specific binding to certain target genes. Here, we discuss which mutations and deletions of the PRC2 complex have been detected in different cancers, with a specific focus on the overexpression of EZH2 in prostate cancer. Abstract : PRC2 in cancer can be mutated leading to activation/inactivation associated with gain or loss of H3K27me3. Overexpressed EZH2 acquires new targets and silences tumor suppressors and miRNAs. Phosphorylated EZH2 can acquire non‐histone substrates. Lastly, PRC2 associated factors can be mutated or affected in cancer modulating PRC2 binding accordingly.