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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.

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

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

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 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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