CHROMATIN & SPLICING

THE ROLE OF EPIGENETICS IN THE REGULATION OF CELL-SPECIFIC ALTERNATIVE SPLICING PROGRAMS

Coordinatore	CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE    more  Organization address address: Rue Michel -Ange 3 city: PARIS postcode: 75794 contact info Titolo: Mr. Nome: Jocelyn Cognome: Mere Email: send email Telefono: +33 4 67613535 Fax: +33 4 67043236
Nazionalità Coordinatore	France [FR]
Totale costo	100˙000 €
EC contributo	100˙000 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2012-CIG
Funding Scheme	MC-CIG
Anno di inizio	2014
Periodo (anno-mese-giorno)	2014-01-01   -   2017-12-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE  Organization address address: Rue Michel -Ange 3 city: PARIS postcode: 75794 contact info Titolo: Mr. Nome: Jocelyn Cognome: Mere Email: send email Telefono: +33 4 67613535 Fax: +33 4 67043236	FR (PARIS)	coordinator	100˙000.00

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 Obiettivo del progetto (Objective)

'Re-differentiation of carcinogenic epithelial cells to mesenchymal by epithelial-to-mesenchymal transition (EMT) confers properties to tumour cells, which turn them highly metastatic and resistant to chemotherapy. Traditionally, it was thought that expression of key genes was enough to induce EMT. However, very recently, alternative processing of transcribed genes into different matured mRNAs, and therefore proteins, by alternative splicing has also been implicated in EMT progression. Even more, switches in cancer-specific splicing isoforms to normal variants have been shown to reduce tumorigenicity and revert EMT. In parallel, recent observations point to an important regulatory role of chromatin structure and ncRNAs in modulating alternative splicing. This project aims to combine these new concepts to uncover, for the first time, the role of epigenetics in the regulation of cell-specific splicing programs in an inducible, physiologically relevant EMT cell reprogramming system. I will, first, probe at a gene-specific and genome-wide level the role of DNA and histone modifications in the establishment and maintenance of a new EMT-induced splicing program. Then, using a high-throughput screening approach, I will identify and characterize novel miRNAs and chromatin-based regulators of EMT-mediated alternative splicing that will be functionally tested for their capacity to impair EMT. This multidisciplinary project integrates novel concepts and challenging approaches in the field of epigenetics, ncRNA, splicing and cancer biology that will bring, conceptually and mechanistically, new insights into alternative splicing regulation and how cancer-specific splicing programs are established and maintained. In the long-term, this study has the potential to discover unexpected and innovative new molecular mechanisms of splicing regulation that can be applied for predicting and restoring cell-specific splicing patterns by mapping and modulating epigenetic modifications.'