Laurent CORCOS
  • E-mail :[email]
  • Phone : 33 2 98 01 83 01
  • Location : Brest, France
Last update 2011-08-23 10:43:31.27

Laurent CORCOS PhD Biomedical Research

Course and current status


Born 01/01/1960                                                                                   


Faculty of Medicine,

22 Avenue Camille Desmoulins

29200 BREST, FRANCE                                                                                               


Diplomas and academic cursus

1988: PhD (Paris VI, Pasteur Institute, supervisor:Dr MC Weiss)

1990: INSERM Position

1990-1992: Post-doctoral training (McArdle Laboratory for Cancer Research, Madison, WI, USA, supervisor: Pr N. Drinkwater)

1995: CESAM diploma (Statistics applied to medicine)

1997: Research Directorship

2006: Inserm Research Director


10/1992-12/1998: Inserm Unit 49, then Unit 456 (Rennes)

01/1999-08/2004: Inserm Unit 517 (Dijon).

09/2004-: Inserm Unit 613 (Brest)


Areas of interest

Cancer Biology

Cell Death

Pre-mRNA splicing




Scientific summary

I obtained my PhD from the Pasteur Institute (1988). I studied liver differentiation with the Reuber rat hepatoma cell system. I followed with studies aimed at analysing the regulation of expression of detoxication enzymes, such as cytochromes P450, by Phenobarbital and dexamethasone (1986-1993). We were the first to show that the antiprogestin RU486 mimicked the inductive effect of Phenobarbital in hepatoma cells. It was later shown that this effect was due to activation of two nuclear receptors, the Constitutive Androstane Receptor (CAR) or the Pregnane X Receptor (PXR).

Then I studied the interaction between inflammatory mediators, like IL1b, IL6, TNFa or TGFb, or anti-inflammatory cytokines like IL4 (1993-1996). We showed that the pro-inflammatory cytokines reduced cytochrome P450 expression in human hepatocytes, whereas IL4 was unique in inducing cytochrome P4502E1, the ethanol-inducible enzyme. We also cloned several mouse cytochromes P450 from the 2b family, and showed, by a genetic analysis in mice, that Phenobarbital induction of cytochrome P4502b10 was regulated by one major chromosomal locus (1995-1998). Recently, we also got involved in the study of human cytochromes P4504A and 4F, among others, using the liver hepatoma cell line HepaRG, both from a biochemical and biological perspective (2006-2009).

I also studied apoptosis in human cells and we were the first group to clone the human Caspase-2 gene (before the availability of the human genome sequence), and went on to describe its transcriptional regulation as well as the regulation of its alternative pre-mRNA splicing brought about by DNA damaging agents (2003-2008). We also showed that caspase-2 played a role independent of its activity in apoptosis, in lipid anabolism through its regulation by Sterol Regulatory Element Binding Proteins (SREBP). We also showed that human caspase-7 was also regulated by lipid levels, through SREBP (2009).

We also built the first bioinformatics model of the cholesterol synthesis pathway using Boolean equations and an adaptation of Markov chains (2008).

We studied alternative pre-mRNA splicing of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene, and showed that the ETR-3 splice protein, which was known to be active mainly in muscles, was a novel regulator of CFTR pre-mRNA splicing in epithelial cells (2010).

We also studied the effect of DNA damaging agents on the coupling between transcription and pre-mRNA splicing, and we showed that the molecular dialogue between both machineries involved YB1and EWS (2010). The interaction was disrupted upon DNA damage, which led to a profound modification of the splicing machinery, with a rather massive effect on MDM2 alternative pre-mRNA splicing.

We now follow two main paths: firstly, we survey apoptosis endpoints as a response to blunting the mevalonate (cholesterol) pathway. Secondly, we perform large-scale analyses of alternative pre-mRNA splicing using Exon Array gene chips in human digestive tract diseases. We will then integrate all these data with the aim to model the associated events in human cancer.

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