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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.

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

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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