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SPLICANCER SIGNED

Regulation and reprogramming of alternative splicing in cellular transformation

Total Cost €

EC-Contrib. €

Partnership

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Outcomes and
results

SPLICANCER project word cloud

Explore the words cloud of the SPLICANCER project. It provides you a very rough idea of what is the project "SPLICANCER" about.

mechanisms splicing protein transformation stem vitro biochemical preliminary endocytosis proliferative beahviour intends instrumental oncogenic regulation aberrantly critical genes reprogramming off assayes tumour switch establishment sequences epithelial migration revealed found spectrometry reported selective isoforms dictates lab percent multidisciplinary basis host nearly myosin cell deregulation mutations progression alternative de vishort skipping molecular human characterisation functions little suggest culture diseases evidences regulated expression possibly regulators polarized disrupt model isoform diversity advantage exon addiction gained regulatory biological interactome cancer express architecture vi cells events cellular mechanism somatic modulates contributor mass source deregulated

Project "SPLICANCER" data sheet

The following table provides information about the project.

Coordinator	IFOM FONDAZIONE ISTITUTO FIRC DI ONCOLOGIA MOLECOLARE Organization address address: VIA ADAMELLO 16 city: MILANO postcode: 20139 website: www.ifom-firc.it contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.
Coordinator Country	Italy [IT]
Project website	https://www.ifom.eu/en/cancer-research/research-labs/research-lab-polo.php
Total cost	168˙277 €
EC max contribution	168˙277 € (100%)
Programme	1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
Code Call	H2020-MSCA-IF-2016
Funding Scheme	MSCA-IF-EF-ST
Starting year	2017
Duration (year-month-day)	from 2017-07-01 to 2019-06-30

Partnership

Take a look of project's partnership.

#	participants	country	role	EC contrib. [€]
1	IFOM FONDAZIONE ISTITUTO FIRC DI ONCOLOGIA MOLECOLARE IFOM FONDAZIONE ISTITUTO FIRC DI ONCOLOGIA MOLECOLARE Organization address address: VIA ADAMELLO 16 city: MILANO postcode: 20139 website: www.ifom-firc.it contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.	IT (MILANO)	coordinator	168˙277.00

Map

Project objective

Alternative splicing (AS), by affecting nearly 90 percent of human genes, is the major contributor to protein diversity. Mutations that disrupt AS regulatory sequences are a widespread source of human diseases. Various evidences suggest that an AS reprogramming is critical in cell adaptation during cancer development. In spite of increasing interest in the potential oncogenic role of AS, little is known about the molecular mechanisms behind its deregulation during the somatic to the cancer cell transformation. Our aim is to contribute to the characterisation of AS reprogramming during the somatic to the proliferative cancer cell transformation using myosin VI as model system. Recent studies from the host lab reported how myosin VI AS modulates its interactome leading to different cellular functions (endocytosis for the long isoform and cell migration for the short one). The lab found that alternative myosin VI splicing is aberrantly regulated in cancer, where exon skipping dictates cell addiction to myosin VIshort for tumour cell migration.In this proposal, we intends to 1) Identify the myosin VI’s alternative splicing regulators and define their role in vitro, 2) identify common splicing-regulated events that occur during the establishment of a fully polarized epithelial architecture and that are possibly deregulated in cancer (AS reprogramming), 3) assess whether cancer stem cells express a specific set of the identified AS genes.Preliminary results revealed that myosin VI isoforms expression can be switch on/off in selective culture conditions. We will take advantage of this beahviour to set up our analysis based on a multidisciplinary approach that includes biochemical, mass spectrometry and cellular biological assayes. The new set of information will gained with this proposal will be instrumental to understanding the molecular mechanism at the basis of AS (de)regulation for myosin VI and more in general for cell transformation during cancer progression.

Publications

List of publications.
year	authors and title	journal	last update
2018	Carlos A. NiÃ±o, Simona Sala, Simona Polo When ubiquitin meets E-cadherin: Plasticity of the epithelial cellular barrier published pages: , ISSN: 1084-9521, DOI: 10.1016/j.semcdb.2018.12.005	Seminars in Cell & Developmental Biology	2019-08-29

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