HORAY

Role of Autophagy and Lysosomal Biogenesis in Hypoxia and Radiation-induced cell death in normal and cancer cells

 Coordinatore THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD 

 Organization address address: University Offices, Wellington Square
city: OXFORD
postcode: OX1 2JD

contact info
Titolo: Ms.
Nome: Gill
Cognome: Wells
Email: send email
Telefono: +44 1865 289800
Fax: +44 1865 289801

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 231˙283 €
 EC contributo 231˙283 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2012-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-09-01   -   2015-08-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD

 Organization address address: University Offices, Wellington Square
city: OXFORD
postcode: OX1 2JD

contact info
Titolo: Ms.
Nome: Gill
Cognome: Wells
Email: send email
Telefono: +44 1865 289800
Fax: +44 1865 289801

UK (OXFORD) coordinator 231˙283.20

Mappa


 Word cloud

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

cancer    ask    sensitivity    pathways    radiation    lines    hypoxia    breast    biogenesis    tfeb    ionizing    toxicity    autophagic    cells    cell    screen    variants    autophagy    normal    moderate    conduct    sirna    lysosomal    throughput   

 Obiettivo del progetto (Objective)

'The aims of the project are to investigate, for the first time, the mechanisms and the role of autophagy and lysosomal biogenesis in hypoxia and radiation-induced cell death in normal and cancer cells. In project 1 we ask whether autophagy and lysosome biogenesis are involved in hypoxia and the acute and/or late toxicity of radiation in normal cells and tissues, and the eventual radioprotection that could be achieved by modifying process. We will study the direct effects of ionizing radiation and hypoxia on the autophagic pathway and lysosomal biogenesis in normal cell lines. Also, we will conduct a moderate-throughput siRNA screen of different autophagic variants and lysosomal biogenesis pathways in hypoxia and radiation in normal cells. Further, we will study the effects of ionizing radiation in liver conditional knockout or overexpressed mouse line of the master transcriptional regulator of autophagy and lysosomal biogenesis TFEB, and compare its radiation toxicity with the commercial available compound the amifostine. In project 2 we ask whether upregulation or downregulation of the autophagy and lysosomal biogenesis could enhance the radiation sensitivity in vitro and in vivo. We will identify mutants in fission yeast that are either protective from, or synergistic with ionizing radiation and link with autophagy and lysosomal biogenesis and will be further exam in breast cancer cell lines. We will conduct a moderate-throughput siRNA screen of different autophagic variants and lysosomal biogenesis pathways in radiation sensitivity in breast cancer cell lines. Also we will develop an inducible dox-shRNA for TFEB in a xenograft model and investigate the therapeutic value combined with radiation therapy. We anticipated to identify critical targets for pharmacological or molecular interventions aiming to selective protection of normal cells and enhancement of the efficacy of radiotherapy and/or chemotherapy of tumors.'

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