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IEOCCD SIGNED

THE IMPACT OF THE ENVIRONMENT AND ONCOGENESIS ON CANCER CELL DIVISIONS

Total Cost €

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EC-Contrib. €

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Partnership

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Project "IEOCCD" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITY COLLEGE LONDON 

Organization address
address: GOWER STREET
city: LONDON
postcode: WC1E 6BT
website: n.a.

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]
 Total cost 212˙933 €
 EC max contribution 212˙933 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2019
 Duration (year-month-day) from 2019-05-01   to  2021-04-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITY COLLEGE LONDON UK (LONDON) coordinator 212˙933.00

Map

 Project objective

Mammalian cells must round up to divide by remodeling their adhesions and their cytoskeleton to form a stiff actin cortex. Mitotic rounding provides the space necessary to develop a mitotic spindle to undergo symmetric chromosomal segregation. If mitotic rounding is impeded by physical confinement or preventing adhesion remodeling, defects in spindle assembly and chromosomal missegregation can lead to mitotic cell death. In cancer, the cells must divide in a challenging environment which can alter the way cells divide. Preliminary data show Ras- activated epithelial cells are able to round better compared to normal cells. This adaptation could protect the dividing cell from the physical environment and allow epithelial cancer cells to divide in the confines of the tumor and distant metastatic sites. Here, we aim to identify mechanisms that allow epithelial cancer cells to divide differently from that of normal epithelial cells. Potentially, this mechanism could be a powerful target if we are able to prevent cancer cell division without interfering with normal cell division. Preliminary data suggest Ras-ERK signalling could play a role in mitotic rounding of cancer cells. In this proposal, I will 1) investigate ERK signalling dynamics during mitotic progression, how it regulates mitotic rounding and effects on the following cell cycle 2) investigate how Ras-ERK signalling and the mechanism of cell division are affected by environment using microfabricated tools and 3) initiate oncogenic activation by over-expressing receptor tyrosine kinases commonly found over-expressed in cancer or constitutive activation of Ras/Raf and measure changes in Ras-ERK signalling and cell mechanics. By establishing a link between Ras-ERK signalling and mitotic progression, I will determine how oncogenesis affects Ras-ERK signalling dynamics and cell division to allow cancer cells to divide in a wide range of environments.

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

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