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Cdc42Adhere

Role of Cdc42 in cancer cell adhesion to endothelial cells and platelets

Total Cost €

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EC-Contrib. €

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Partnership

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Project "Cdc42Adhere" 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 https://kclpure.kcl.ac.uk/portal/en/projects/role-of-cdc42-in-cancer-cell-adhesion-to-endothelial-cells-and-platelets-cdc42adhere
 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 2015
 Duration (year-month-day) from 2015-05-11   to  2017-05-10

 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

Metastasis accounts for 90% of cancer deaths, and it is therefore important and timely to identify new therapeutic targets aimed specifically at metastasis. Cdc42 has recently been implicated in a key step of the metastatic cascade: the extravasation of circulating tumour cells, also termed transendothelial migration (TEM) . This project aims to study how Cdc42 contributes to breast cancer cell TEM in vitro and in vivo. Cdc42 regulates β1‐integrin expression via the transcription factor serum response factor (SRF) and thereby stimulates cancer cell adhesion to endothelial cells (ECs) and TEM. To analyse the molecular basis for this regulation, downstream targets of Cdc42 will be depleted by RNAi in a panel of breast cancer cells to determine which target/s are responsible for altering β1‐integrin expression, adhesion to ECs or TEM. Cancer cells interact with platelets as soon as they enter the bloodstream, and this enhances cancer cell TEM in vivo. It is therefore possible that Cdc42 regulates attachment to platelets as well as ECs. The role of Cdc42 in the interaction between platelets and cancer cells will be tested by adding purified platelets to control or Cdc42‐depleted breast cancer cells in vitro and analysing platelet aggregation around cancer cells by confocal microscopy. The role of Cdc42 in platelet attachment to cancer cells during early lung colonization in vivo will be studied by intravenous injection of fluorescently tagged breast cancer cells in mice. This project will increase our understanding of metastasis. The identification of molecular targets involved in cancer cell extravasation will provide a starting point for the development of new drugs, thus contributing to reduce the mortality of patients with metastasis.

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The information about "CDC42ADHERE" are provided by the European Opendata Portal: CORDIS opendata.

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