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GENMETASTEM SIGNED

GENOMIC AND METABOLIC REGULATION OF METASTATIC CANCER STEM CELLS

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 GENMETASTEM project word cloud

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

mode    therapies    self    carcinoma    relapse    unexplored    cell    maintained    spread    traits    closely    contractility    deaths    triggered    metabolism    tumour    differentiate    regulated    movement    prognostic    markers    understand    cscs    renewal    successfully    mat    stemness    transition    imaging    preliminary    combines    linked    invasion    resistance    emt    vivo    hypothesize    nevertheless    shows    migration    elongated    metastasis    lab    host    functionally    cancer    regulates    rho    regulating    interestingly    biology    clues    interdisciplinary    initiation    amoeboid    actomyosin    models    epithelial    regulate    biochemistry    cytoskeletal    organs    drug    cells    breast    glutamine    data    genes    contractile    participate    molecular    mediated    signalling    types    regulation    stem    unravelling    animal    rock    link    metabolic    acquire    acquisition    melanoma    cellular    suggesting    mesenchymal    distant    metastatic    metastasize    techniques    ultimate    correlates    cues    renew    causes   

Project "GENMETASTEM" data sheet

The following table provides information about the project.

Coordinator
KING'S COLLEGE LONDON 

Organization address
address: STRAND
city: LONDON
postcode: WC2R 2LS
website: www.kcl.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 http://www.kcl.ac.uk
 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-2014
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2016
 Duration (year-month-day) from 2016-09-01   to  2018-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KING'S COLLEGE LONDON UK (LONDON) coordinator 183˙454.00

Map

 Project objective

The major causes of cancer deaths are relapse and resistance to current therapies associated with the presence of cancer stem cells (CSCs) and metastatic growth in distant organs. CSCs have the ability to self-renew and differentiate in non-CSCs. In breast cancer, acquisition of stemness properties has been closely related to epithelial-mesenchymal transition (EMT), a key process in cancer invasion and metastasis triggered via Rho-ROCK mediated actomyosin contractility. Interestingly, in melanoma, transition from elongated-mesenchymal to amoeboid mode of movement (MAT) driven by Rho-ROCK signalling has been associated with increased stemness. Furthermore, preliminary data from host lab shows that actomyosin cytoskeletal regulates glutamine metabolism in both melanoma and breast cancer cells. Metabolic cues participate in stem cell self-renewal regulation, suggesting that, in very contractile cells, the regulation of EMT, metastatic spread and tumour initiation might be functionally linked to stemness via metabolic clues. Nevertheless, how very contractile cells regulate genes involved in all these processes remains unexplored. As increasing contractility via EMT in carcinoma cells or via MAT in melanoma cells correlates with increasing stemness, we hypothesize a molecular link between the pathways regulating both migration and stemness abilities, which will be maintained across tumour types (from carcinoma to melanoma). The main goal of this proposal is to understand how tumour cells can acquire stem cell traits to successfully metastasize and how this can be regulated by the actomyosin cytoskeletal by using an interdisciplinary approach that combines state-of-the-art techniques in molecular and cellular biology, biochemistry, in vivo imaging and animal models. This will allow to identify key important genes regulating both stemness traits and metastatic spread with the ultimate goal of unravelling novel drug targets and prognostic markers of distant relapse.

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The information about "GENMETASTEM" are provided by the European Opendata Portal: CORDIS opendata.

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