Speaker: Jesús Gil
Cell Proliferation Group
MRC Clinical Sciences Centre
Imperial College Faculty of Medicine, London, UK

Host

Eduard Batlle, IRB Barcelona

Tuesday, 17 June 2008, 12.00h Aula Fèlix Serratosa

Abstract

Cellular senescence is an irreversible growth arrest that accompanies the replicative exhaustion of normal cells in culture. A similar response, termed oncogene-induced senescence (OIS), is triggered when cells suffer inappropriate oncogenic signalling. During tumourigenesis, an enrichment of senescent cells is notorious in some pre-neoplastic lesions, like lung adenomas and papillomas or nevi in the skin. This observation together with the fact that mutations disabling senescence are needed to cooperate in cancer progression suggest that senescence constitutes a tumour suppressor mechanism.

Our lab is interested in the identification of genes influencing senescence. To this end, a general approach that we take is to perform genetic screens. Taking this approach we have discovered novel regulators of senescence, such as CBX7 or CXCR2. CBX7 is a Polycomb gene that contributes to senescence bypass through the transcriptional repression of the INK4a/ARF locus and it is an oncogene involved in follicular lymphoma. More recently, we have identified the chemokine receptor CXCR2 as part of a self-amplifying chemokine network involved in senescence reinforcement. Interestingly the expression of CXCR2 is elevated in preneoplastic lesions in vivo, and there are hints that suggest that CXCR2 could have a tumour suppressive role at early stages of cancer progression.

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