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Help us improve our products. Sign up to take part. A Nature Research Journal. Dysregulation of histone modifications promotes carcinogenesis by altering transcription.
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However, the role of EZH2 in this setting is unclear due to the context-dependent functions of PRC2 and the heterogeneity of breast cancer. Moreover, the mechanisms underlying PRC2 overexpression in cancer are obscure.
Here, using multiple models of breast cancer driven by the oncogene ErbB2, we show that the tyrosine kinase c-Src links energy alison with PRC2 overexpression via control of mRNA translation. We show that Ezh2 overexpression and activity are pivotal in ErbB2-mediated mammary tumourigenesis.
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A nude regulator of pluripotency and differentiation 23PRC2 also has a complex role in cancer, with gain and loss-of-function mutations in PRC2 components reflecting context-specific oncogenic and tumor suppressive activities 4. Some cancers also overexpress PRC2 components 4increasing the likelihood that PRC2 will bind chromatin at transiently repressed loci to enforce stable transcriptional silencing 4.
Thus, under conditions where PRC2 exerts oncogenic effects, its overexpression may facilitate tumorigenesis in the absence of activating mutations of its components.