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INTEGRISTEM TERMINATED

Functions of Integrins in Mammary Stem Cell Activity and Tumorigenesis

Total Cost €

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EC-Contrib. €

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Partnership

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 INTEGRISTEM project word cloud

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

interactions    originate    epithelial    cells    bipotent    notably    capacity    mouse    mammary    alveolar    progenitors    membrane    niche    pregnancy    stages    breast    differentiation    drastic    indicated    mutant    normal    brca1    creloxp    activated    developmental    bilayer    restricted    thought    stem    organotypic    clonogenic    layers    model    maintenance    mice    tumorigenesis    analyze    tumors    whilst    binding    myoepithelial    examined    producing    milk    cell    laminin    expression    morphogenesis    cancer    abnormal    organization    basement    chains    survival    progenitor    receptors    expansion    p53    apical    depleted    baso    alpha    layer    integrins    understanding    deleted    initiation    vivo    virgin    function    lobulo    cytoskeleton    appear    regenerative    regulation    cultures    epithelium    gland    contain    hormones    ex    promoter    biologists    populations    basal    tested    amplification    cre    puberty    adult    polarization    employed    elucidate    blg    proliferation    molecular    luminal    functional    microenvironment    glands    tumor    lineage    integrin    population    mutations   

Project "INTEGRISTEM" data sheet

The following table provides information about the project.

Coordinator
INSTITUT CURIE 

Organization address
address: rue d'Ulm 26
city: PARIS
postcode: 75231
website: www.curie.fr

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 France [FR]
 Project website https://science.institut-curie.org/research/multiscale-physics-biology-chemistry/umr144-subcellular-structure-and-cellular-dynamics/team-glukhova/
 Total cost 185˙076 €
 EC max contribution 185˙076 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2015
 Funding Scheme MSCA-IF-EF-RI
 Starting year 2016
 Duration (year-month-day) from 2016-05-01   to  2018-04-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    INSTITUT CURIE FR (PARIS) coordinator 185˙076.00

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 Project objective

Understanding the functional interactions between mammary epithelium and its microenvironment, with a particular focus on the stem cell niche, represents a challenge for developmental and cancer biologists. Mammary epithelium is a bilayer, with a layer of luminal cells, producing milk, and a layer of basal myoepithelial cells. Both layers contain clonogenic stem/progenitor cells, which ensure the drastic epithelial expansion in puberty and pregnancy. Whilst basal stem cells are thought to be bipotent, luminal progenitors appear to be lineage-restricted in normal gland. Recent studies indicated that basal-like breast tumors, notably those with BRCA1 mutations, might originate from luminal progenitors. Our project aims to elucidate the role of integrin receptors for Laminin, major component of the mammary basement membrane, in the regulation of the luminal progenitor function during normal mammary development and tumorigenesis. To this end, α3 and α6 integrin chains were deleted from mammary luminal cells in vivo using CreLoxP system. Cre expression was driven to luminal progenitors by the Blg promoter, activated in this cell population in adult virgin mice and further on, during lobulo-alveolar development in pregnancy. The stem cell activity and the maintenance of the stem cell populations in mutant mammary glands will be analyzed at different developmental stages. Morphogenesis, proliferation, survival, differentiation as well as the regenerative and clonogenic potential of the mutant epithelium will be examined. We will study the cytoskeleton organization and the capacity of mutant cells for baso-apical polarization. To analyze the responses of integrin-depleted cells to hormones and growth factors at the molecular level, organotypic ex vivo cultures will be employed. The impact of Laminin-binding integrins on abnormal luminal progenitor amplification during tumor initiation will be tested in a mouse model of basal-like breast cancer induced by p53 and BRCA1 loss.

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