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前列腺癌中PRC2的突变与缺失

Mutations and deletions of PRC2 in prostate cancer.

作者信息

Jain Payal, Di Croce Luciano

机构信息

Centre for Genomic Regulation (CRG), Barcelona Institute of Science and Technology, Barcelona, Spain.

Universitat Pompeu Fabra (UPF), Barcelona, Spain.

出版信息

Bioessays. 2016 May;38(5):446-54. doi: 10.1002/bies.201500162. Epub 2016 Mar 22.

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.

摘要

多梳蛋白家族(PcGs)是转录抑制复合物,可调节重要的生物学过程并在癌症中发挥关键作用。EZH2的突变或缺失可通过增加或减少H3K27me3而同时具有致癌和抑癌功能。相比之下,据报道SUZ12和EED的突变具有抑癌功能。EZH2在包括前列腺癌在内的许多癌症中过度表达,这可导致肿瘤抑制因子、调节上皮-间质转化(EMT)的基因以及干扰素信号通路沉默。在某些情况下,EZH2的过度表达还会导致其使用非组蛋白底物。最后,PRC2相关因子可通过渐进性突变或通过与某些靶基因的特异性结合来影响癌症进展。在此,我们讨论了在不同癌症中检测到的PRC2复合物的哪些突变和缺失,特别关注EZH2在前列腺癌中的过度表达。

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