Dr Eric Chevet; Inserm
Eric Chevet is Research Director at the French National Institute for Health and Medical Research (Inserm). After a Ph.D. in Molecular Cell Biology from the University of Paris XI in 1996 and a post-doctoral fellowship at McGill University (Canada), he established his own laboratory at McGill University in 2001 before going back to France in 2006. For the past 20 years he has been investigating the role of endoplasmic reticulum stress signalling and Proteostasis control in cancer development. Early 2015, he moved to Rennes in the West part of France to head a Cancer Research Laboratory within the Comprehensive Cancer Centre Eugène Marquis (INSERM U1242,University of Rennes). The main objective of this research centre will be to characterize select stress signalling pathways (including ER stress, death receptors, DNA damage) in various cancers and develop novel relevant therapeutics to impede cancer development. Eric Chevet has authored > 240 publications, few patents, and is a founder of Thabor Therapeutics and Exa Noma Therapeutics. He is an editor of the FEBS Journal and of Proteostasis.
Proteostasis imbalance is emerging as a major hallmark of cancer, driving tumour aggressiveness. Genetic and pharmacological evidence have suggested that the endoplasmic reticulum (ER), a major site for secretory and transmembrane protein folding and quality control, plays a critical role in cancer development. This concept has been validated in triple negative breast cancer, prostate cancer as well as in glioblastoma (GB), the most lethal primary brain cancer with an overall survival of 15 months and no effective treatment. We demonstrated that the ER stress sensor IRE1 contributes to GB progression, impacting tissue invasion and tumour vascularization. IRE1is a dual Kinase/RNase that signals by catalysing the non-conventional splicing of the mRNA encoding the transcription factor XBP1, and in addition by regulating RNA stability through a process known as Regulated IRE1 Dependent Decay (RIDD). We have identified IRE1as an actionable therapeutic target and we have developed pharmacological approaches to increase the efficacy of GB standard of care in mouse models. At last, we have investigated the molecular mechanisms by which IRE1 contributes to tumour development and how its inhibition can improve the tumour response to the combined action of irradiation and chemotherapy with temozolomide through the unexpected modulation of lipid metabolism and DNA repair.
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