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Rewiring transcriptional regulation by the PRC2 complex using proximity inducing pharmacology

Project description

Targeting epigenetics in cancer

During cancer development, cells accumulate both genetic and epigenetic alterations. The latter include chemical modifications of DNA and histones and impact the expression of genes such as tumour-suppressor genes. polycomb repressive complex 2 (PRC2) participates in gene silencing in cancer and its inhibition constitutes a promising therapeutic target. Funded by the Marie Skłodowska-Curie Actions programme, the Rewiring PRC2 project will use cutting-edge techniques to identify effectors that can rewire PRC2 function. The work will lead to novel compounds for cancer therapy that can inhibit PRC2 and derepress silenced tumour-suppressor genes.

Objective

Polycomb repressive complex 2 (PRC2), which incorporates repressive methyl-lysine marks on histone H3 to facilitate global transcriptional repression, is an integral epigenetic modifier in normal development. Components of this complex, especially EZH2, are hyperactive or overexpressed in a broad range of cancers, resulting in excessive silencing of tumor suppressor genes (TSGs). Moreover, cancers with defects in the SWI/SNF complex, the most frequently mutated chromatin regulatory complex in cancer, are dependent on PRC2 function for survival. While inhibition or degradation of PRC2 components have become extremely attractive approaches to cancer therapy, they still suffer from suboptimal kinetics and perturbation because they must rely on opposing epigenetic modifiers and transcriptional regulators to derepress expression of silenced TSGs. Thus, I aim to overcome this issue by leveraging the cancer driver itself to derepress silenced TSGs. In this regard, I will utilize a high-throughput protein recruitment screen, coupled to next-generation sequencing, to identify proteins (effectors) that, when recruited to PRC2, can rewire its function to directly derepress a PRC2-silenced locus. This screen will be used a base to develop novel proximity inducing compounds, which can rewire the function of PRC2. The compound that produces the strongest transcriptional derepression and anti-proliferative effects in cancer cells will then be characterized via transcriptomics, and chromatin profiling to determine its effects on endogenous gene expression. Ultimately, this study will establish a new class of PRC2 targeting compounds that will pave the way for improved cancer therapies, which both inhibit PRC2 methyltransferase activity and directly derepress PRC2-silenced TSGs.

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HORIZON-TMA-MSCA-PF-EF - HORIZON TMA MSCA Postdoctoral Fellowships - European Fellowships

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Call for proposal

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(opens in new window) HORIZON-MSCA-2023-PF-01

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Coordinator

CEMM - FORSCHUNGSZENTRUM FUER MOLEKULARE MEDIZIN GMBH
Net EU contribution

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€ 199 440,96
Address
LAZARETTGASSE 14 AKH BT 25.3
1090 Wien
Austria

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Region
Ostösterreich Wien Wien
Activity type
Private for-profit entities (excluding Higher or Secondary Education Establishments)
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Total cost

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