THE METAENDOMATRIX

THE ENDOCYTIC AND CYTOSKELETAL MATRIX IN THE PLASTICITY OF TUMOR CELL INVASION AND MIGRATION

 Coordinatore IFOM FONDAZIONE ISTITUTO FIRC DI ONCOLOGIA MOLECOLARE 

Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.

 Nazionalità Coordinatore Italy [IT]
 Totale costo 2˙232˙200 €
 EC contributo 2˙232˙200 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2010-AdG_20100317
 Funding Scheme ERC-AG
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-08-01   -   2016-07-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    IFOM FONDAZIONE ISTITUTO FIRC DI ONCOLOGIA MOLECOLARE

 Organization address address: "Via Adamello, 16"
city: MILAN
postcode: 20139

contact info
Titolo: Mr.
Nome: Carlo
Cognome: Raimondi Cominesi
Email: send email
Telefono: +39 02 574303256
Fax: +39 02 574303231

IT (MILAN) hostInstitution 2˙232˙200.00
2    IFOM FONDAZIONE ISTITUTO FIRC DI ONCOLOGIA MOLECOLARE

 Organization address address: "Via Adamello, 16"
city: MILAN
postcode: 20139

contact info
Titolo: Prof.
Nome: Giorgio
Cognome: Scita
Email: send email
Telefono: +39 02 574303277
Fax: +39 02 574303231

IT (MILAN) hostInstitution 2˙232˙200.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

cells    critical    modes    diverse    plasticity    transcriptional    addition    cell    motility    components    tumor    pathways    matrix    programs    cellular    migration    cancer    mirnas    endocytic    endocytosis   

 Obiettivo del progetto (Objective)

'Tumor cells can adopt different modes of cell motility. The ability to switch between diverse modes of migration enables tumors to adapt to micro-environmental conditions and to metastasize. The critical pathways and cellular processes underlying the plasticity of tumor cell motility have only begun to be identified. Endocytosis, originally thought of as a device to internalize nutrients and membrane-bound molecules, is emerging as a connectivity infrastructure (which we call 'the Endocytic Matrix') of different cellular networks necessary for the execution of various cellular programs. A primary role of the Endocytic Matrix is the delivery of space- and time-resolved signals to the cell, and it is thus essential for the execution of polarized functions during cell migration. The molecular mechanisms it uses are, however, ill defined and likely to involve, in addition to extranuclear pathways, also transcriptional programs. In this respect, we have acquired evidence that components of the Endocytic Matrix require de novo gene expression to promote the transition in the mode of tumor cell motility. We propose to identify critical components of the Endocytic Matrix that by controlling the cellular location of actin remodellers promote the plasticity of tumor cell migration. We will also test whether, in addition to the immediate epigenetic/signalling-based control of migration, the Endocytic Matrix regulates transcriptional programs required for the acquisition or maintenance of diverse modes of motility. Finally, in view of the key role of microRNAs (miRNAs) in cancer, we will use miRNA profiling, together with endocytic cell migration and invasion assays in human cancer cells to test whether miRNAs mediate the relationship between endocytosis and motility programs.'

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