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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.

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

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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