IndraLab

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BAP1 inhibits EZH2. 13 / 13
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"To that end, a systematic literature review was performed of articles dealing with a loss of BRCA1-associated protein 1 (BAP1), methylthioadenosine (MTAP), 5-hydroxymethylcitosine (5-hmC), glucose transporter 1 (GLUT1), insulin like-growth factor II messenger RNA-binding protein 3 (IMP3), enhanced zeste homologue 2 (EZH2) staining, cyclin-dependent kinase inhibitor 2A (CDKN2A) homozygous deletion (HD) testing, soluble mesothelin, and microRNA quantification in cytological samples for the diagnosis of MPM versus reactive atypical mesothelial cells."
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"Indeed , we observed that loss of BAP1 results in elevated EZH2 expression and increased H3K27me3 levels , and knock-down of Ezh2 leads to decreased H3K27me3 levels in BNC cells ( Fig. 5 , B and C ; and Fig. S2 J ) ."
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"LaFave et al. [XREF_BIBR] reported that loss of BAP1 promotes MPM cell proliferation by upregulating EZH2."
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"BAP1 loss leads to reduced L3MBTL2 stability and increased EZH2 transcriptional output (XREF_FIG)."
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"Concomitant Bap1 and Ezh2 loss reduced myeloid progenitor expansion, reduced the proportion of Mac1 + Gr1 + myeloid cells, restored erythroid differentiation (CD71 + Ter119 +) and decreased proliferation of Bap1 and Ezh2 deficient progenitors (XREF_FIG and XREF_SUPPLEMENTARY)."
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"BAP1 loss leads to increased expression of EZH2 ( 15 ) ."
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"BAP1 deletion promotes cell proliferation by upregulating enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2)."
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"BAP1 loss also up-regulates the expression of EZH2 , a Polycomb Repressive Complex-2 ( PRC2 ) component involved in epigenetic silencing ( 59 ) and oncogenic pathways ( 60 ) , suggesting sensitivity of BAP1-deficient MPM tumors to EZH2 inhibition ."
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"As for the reported tumor suppressive mechanism, BAP1 can antagonize EZH2 and PRC2 or RING1B (RNF2)/PRC1 in a tissue specific manner."
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"Additionally, reconstitution of BAP1 into the BAP1-KO cells downregulated H3K27me3 and EZH2 (Fig. 2c), suggesting that BAP1 loss might upregulate H3K27me3 and EZH2 and activate their downstream signaling.A recent study indicated that BAP1 is localized in the endoplasmic reticulum (ER) and bound to the type 3 inositol 1, 4, and 5-triphosphate receptor (IP3R3) [22]."
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"Overexpression of EZH2 is reported in a range of malignancies, and a link between BAP1 loss and overexpression of EZH2 suggests a role for the PRC2 pathway and H3K27 hypermethylation in mesothelioma development and progression (122)."
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"Loss of BAP1 has been shown to be synthetically lethal with inhibition of EZH2 or PRC2."
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"Loss of BAP1 leads to reduced L3MBTL2 stability and increased EZH2 transcriptional output in mesothelioma [XREF_BIBR]."
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