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EPILIPRO SIGNED

Elucidating the role of Arid1a in adult liver

Total Cost €

0

EC-Contrib. €

0

Partnership

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Project "EPILIPRO" data sheet

The following table provides information about the project.

Coordinator
THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE 

Organization address
address: TRINITY LANE THE OLD SCHOOLS
city: CAMBRIDGE
postcode: CB2 1TN
website: www.cam.ac.uk

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 United Kingdom [UK]
 Project website https://www.gurdon.cam.ac.uk/research/huch
 Total cost 183˙454 €
 EC max contribution 183˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2015
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2016
 Duration (year-month-day) from 2016-05-01   to  2018-04-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE UK (CAMBRIDGE) coordinator 183˙454.00

Map

 Project objective

Liver cancer is the fifth most common malignancy in men and the eighth in women worldwide. Of note, liver cancer is tightly associated with tissue damage due to the high metabolic and drug detoxification activity of the liver. Increasing evidence demonstrates that toxic agents induce the activation of a resident ductal-progenitor population capable of regenerating the tissue. Therefore, understanding molecular mechanisms governing liver progenitor cells is essential for preventing tumour initiation and progression. The aim of this proposal is elucidating the role of Arid1A (the DNA-binding subunit of the nucleosome-remodelling complex SWI/SNF) in adult liver progenitors by using novel 3D-organoid cultures, which allows long-term expansion of adult ductal-progenitors derived from the healthy liver. Moreover, genome-wide analysis and in vivo approaches will be implemented for accomplishing the goals of the project. Supporting a crucial role for Arid1a in liver progenitors, Arid1a expression is high in organoid cultures and is up-regulated in the adult liver upon damage as compared to the healthy liver. Importantly, Arid1a and other SWI/SNF subunits are mutated in liver cancer, suggesting that Arid1a and SWI/SNF exert a tumour suppression function. In line with this, our preliminary results indicate that depletion of Arid1a and SWI/SNF components increases organoid formation efficiency. Overall, this research plan will shed light on the function of Arid1a and the SWI/SNF nucleosome-remodelling complex in adult liver progenitors and mouse liver regeneration, providing novel hints into their role in carcinogenesis.

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