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MRTFSen SIGNED

MRTF/SRF signalling in regulation of cell senescence and melanoma progression

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 MRTFSen project word cloud

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

import    melanoma    senescent    plays    possibility    co    proliferation    actin    mefs    mouse    proteins    transcription    clearance    prior    microenvironment    models    ageing    activators    resistance    malignant    subcellular    progression    molecular    cell    modulate    senescence    rho    signalling    repair    export    migration    binding    nucleus    gtpases    damaged    invasion    srf    recruitment    direct    metastasis    brafv600e    contractility    pro    mrtf    transcriptional    types    tissue    occurs    cells    shuttling    dynamics    family    encode    association    induces    reveal    benefit    pathologies    anti    immune    hepatocarcinoma    extracellular    induce    arrest    initial    activate    modulation    beneficial    promotes    therapeutic    localization    activation    events    cancer    fibrosis    limiting    model    inhibits    act    adhesion    signals    myocardin    tumour    transformation    depletion    mrtfs    suggests    polymerization    nuclear    therapies    cycle    mechanisms    genes   

Project "MRTFSen" data sheet

The following table provides information about the project.

Coordinator
THE FRANCIS CRICK INSTITUTE LIMITED 

Organization address
address: 1 MIDLAND ROAD
city: LONDON
postcode: NW1 1AT
website: www.crick.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]
 Total cost 224˙933 €
 EC max contribution 224˙933 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2019
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2020
 Duration (year-month-day) from 2020-04-01   to  2022-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE FRANCIS CRICK INSTITUTE LIMITED UK (LONDON) coordinator 224˙933.00

Map

 Project objective

Myocardin-related transcription factors (MRTFs) are G-actin binding proteins which act as transcriptional co-activators Myocardin-related transcription factors (MRTFs) are G-actin binding proteins which act as transcriptional co-activators in association with the transcription factor SRF. MRTF-SRF target genes encode numerous proteins involved in actin dynamics, cell adhesion, migration and contractility. The subcellular localization of the MRTFs is controlled by actin binding which inhibits their nuclear import and promotes their nuclear export. Extracellular signals which activate Rho-family GTPases induce actin polymerization and G-actin depletion, which induces MRTF shuttling to the nucleus and transcriptional activation of MRTF-SRF target genes. The MRTF-SRF pathway activation via Rho plays an important role in cancer cell invasion and metastasis. In addition, in MRTF-SRF signalling inhibits cell senescence in hepatocarcinoma cells which present high Rho activity, but this has not been investigated in other cell types or cancer models. Cell senescence is a process of cell-cycle arrest which typically occurs in ageing, cancer, development or tissue repair, and can facilitate recruitment of immune cells. In the tumour microenvironment, senescent cells can direct events such as therapeutic resistance or metastasis that support malignant progression. In this project we will determine the molecular mechanisms by which MRTF-SRF signalling inhibits cell senescence in MEFs. We also aim to investigate the possibility for it to modulate melanoma progression in the BRafV600E mouse model, where senescence is an initial step prior tumour transformation. Increasing evidence suggests that anti- and pro-senescent therapies can be beneficial also in other pathologies, such as fibrosis, by limiting cell proliferation and allowing clearance of damaged cells. These studies have the potential to reveal new approaches to the modulation of senescence pathways for therapeutic benefit.

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