EU H2020 Project "INTEGRISTEM (Functions of Integrins in Mammary Stem Cell Activity and Tumorigenesis)": description, partecipants, costs and EC-fundings

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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.

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

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

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

INSTITUT CURIE

FR (PARIS)

coordinator

185˙076.00

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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