EZH2 is a marker of aggressive breast cancer and promotes neoplastic transformation of breast epithelial cells

By C. Kleer, Q. Cao, S. Varambally, Ronglai Shen, I. Ota, S. Tomlins, Debashis Ghosh, R. Sewalt, A. Otte, D. Hayes and 5 more. Proceedings of the National Academy of Sciences of the United States of America, 2003

1,715 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/2e2f1a2a6acaa4d1dddec8509ecafd4b15940633

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Citations in the corpus

Phosphorylation of EZH2 activates STAT3 signaling via STAT3 methylation and promotes tumorigenicity of glioblastoma stem-like cells (2013, background): “In a wide range of cancers including GBM, EZH2 is highly expressed and its expression positively correlates with tumormalignancy and invasiveness (Crea et al., 2010; Kleer et al., 2003; Varambally et al., 2002).”
Genetic determinants of cancer metastasis (2007, background): “: EZH2 overexpression is predictive of invasive growth in metastatic prostate and breast cancer”
SUZ12 is required for both the histone methyltransferase activity and the silencing function of the EED-EZH2 complex. (2004, result): “Based Kleer et al., 2003; Varambally et al., 2002), indicating that dysfunctionoftheEED-EZH2complexmaycontributeto on the above results, we conclude that the reconstituted EED-EZH2 complex and the native complex have similar cancer.”
Metastasis: from dissemination to organ-specific colonization (2009, background): “Some of these regulators have been linked to metastasis, including polycomb chromatin remodelling complexe”
Integrative genomic and proteomic analysis of prostate cancer reveals signatures of metastatic progression. (2005, background): “While examining concordant proteomic alterations, interestingly, we found that EZH2, a polycomb group protein that we and others have previously characterized as being overexpressed in aggressive prostate and breast cancer (Kleer et al., 2003; Varambally et al., 2002) was one of the 50 proteins iden”
Suz12 is essential for mouse development and for EZH2 histone methyltransferase activity (2004, background): “Indeed, ectopic expression of EZH2 can promote growth advantage in mouse embryo fibroblasts (MEFs) and can induce cellular transformation and invasive capacity to immortalized human breast epithelial cells (Bracken et al, 2003; Kleer et al, 2003).”
Somatic mutations at EZH2 Y641 act dominantly through a mechanism of selectively altered PRC2 catalytic activity, to increase H3K27 trimethylation. (2011, neutral): “Biotinylated peptides, H3 (1-21) (#12-403), H3 (21-44) (#12-404), H3(21-44)K27(me1) (#12-567), H3(21-44)K27(me2) (#12566), and H3(21-44)K27(me3) (#12-565), were purchased from Upstate Biotechnology.”
Epigenetic antagonism between Polycomb and SWI/SNF complexes during oncogenic transformation (2010, positive): “…proliferation and a decreased capacity to form tumors when transplanted into mice, leading to the proposal of Ezh2 as a possible therapeutic target (Bracken et al., 2003; Croonquist and Van Ness, 2005; Kleer et al., 2003; Simon and Lange, Cancer Cell 18, 316–328, 2008; Varambally et al., 2002).”
The Polycomb Complex PRC2 and its Mark in Life (2011, background): “EZH2 has been reported to be a marker of the aggressive stages of prostate and breast malignancie”
Gene silencing in cancer by histone H3 lysine 27 trimethylation independent of promoter DNA methylation (2008, background): “EZH2 is upregulated in prostate and breast cancers with poor prognosi”