Marc Poirot

Dr. Marc Poirot

INOV, Cancer Research Center of Toulouse, Toulouse, Occitanie, France
orcid

Research Focus & Metrics

Academic Career Length

39Years (1988-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 January 2014 in Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
Verified
Journal Article
Closed access
MRMichel Record
Michel Record
KCKevin Carayon
Kevin Carayon
Marc PoirotMarc Poirot
Marc Poirot
SSSandrine Silvente-Poirot
Sandrine Silvente-Poirot

1 August 2010 in Journal of Lipid Research
Verified
Journal Article
Open access
PDF file
CSCaroline Subra
Caroline Subra
DGDavid Grand
David Grand
KLKarine Laulagnier
Karine Laulagnier
ASAlexandre Stella
Alexandre Stella
GLGerard Lambeau
Gerard Lambeau
MRMichel Record
Michel Record
Caroline Subra, David Grand, Karine Laulagnier, Alexandre Stella, Gérard Lambeau, Michael Paillasse, Philippe De Medina, Bernard Monsarrat, Bertrand Perret, Sandrine Silvente-Poirot, Marc Poirot, Michel Record

1 May 2011 in Biochemical Pharmacology
Verified
Journal Article
Closed access
MRMichel Record
Michel Record
CSCaroline Subra
Caroline Subra
SSSandrine Silvente-Poirot
Sandrine Silvente-Poirot
Marc PoirotMarc Poirot
Marc Poirot

1 August 2018 in Journal of Lipid Research
Verified
Journal Article
Open access
PDF file
MRMichel Record
Michel Record
SSSandrine Silvente-Poirot
Sandrine Silvente-Poirot
Marc PoirotMarc Poirot
Marc Poirot
MWMichael J.O. Wakelam
Michael J.O. Wakelam
Intercellular communication has been known for decades to involve either direct contact between cells or to operate by spreading molecules such as cytokines, growth factors, or lipid mediators. Through the last decade we have begun to appreciate the increasing importance of intercellular communication mediated by extracellular vesicles released by viable cells either from plasma membrane shedding microvesicles, also named microparticles), or from an intracellular compartment (exosomes). Exosomes and microvesicles circulate in all biological fluids and can trigger biological responses at distance. Their effects include a large variety of biological processes such as immune surveillance, modification of tumor microenvironment, or regulation of inflammation. They carry a large set of active molecules, including lipid mediators such as eicosanoids, proteins and nucleic acids, able to modify the phenotype of receiving cells. This review will highlight the role of the various lipidic pathways involved in the biogenesis and functions of microvesicles and exosomes.

28 March 2014 in Science
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Journal Article
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SSSandrine Silvente-Poirot
Sandrine Silvente-Poirot
Marc PoirotMarc Poirot
Marc Poirot
Mammalian cells synthesize cholesterol through a series of 21 enzymatic steps, generating numerous metabolites that are involved in the control of physiological and developmental processes. Cholesterol itself is the precursor of steroid hormones and sterols, the latter of which can be further modified into molecules that induce specific biological responses. Epidemiological studies have investigated the role of cholesterol in breast cancer risk, with contradictory findings. Recent studies, however, linking cholesterol metabolism to breast cancer may provide some insights. Certain cholesterol metabolites can promote (1, 2) or suppress (3) breast cancer. This raises the important question of how to regulate or inhibit the cholesterol metabolic pathway, and at which steps, in a therapeutic approach to cancer.

14 May 2013 in Nature Communications
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Journal Article
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PMPhilippe de Medina
Philippe de Medina
MPMichael R. Paillasse
Michael R. Paillasse
GSGregory Segala
Gregory Segala
MVMaud Voisin
Maud Voisin
LMLoubna Mhamdi
Loubna Mhamdi
Marc PoirotMarc Poirot
Marc Poirot
We previously synthesized dendrogenin A and hypothesized that it could be a natural metabolite occurring in mammals. Here we explore this hypothesis and report the discovery of dendrogenin A in mammalian tissues and normal cells as an enzymatic product of the conjugation of 5,6α-epoxy-cholesterol and histamine. Dendrogenin A was not detected in cancer cell lines and was fivefold lower in human breast tumours compared with normal tissues, suggesting a deregulation of dendrogenin A metabolism during carcinogenesis. We established that dendrogenin A is a selective inhibitor of cholesterol epoxide hydrolase and it triggered tumour re-differentiation and growth control in mice and improved animal survival. The properties of dendrogenin A and its decreased level in tumours suggest a physiological function in maintaining cell integrity and differentiation. The discovery of dendrogenin A reveals a new metabolic pathway at the crossroads of cholesterol and histamine metabolism and the existence of steroidal alkaloids in mammals.