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<publisher>HAL CCSD</publisher>
<title lang=en>Role for the ATPase inhibitory factor 1 in the environmental carcinogen-induced Warburg phenotype</title>
<creator>Hardonnière, Kévin</creator>
<creator>Fernier, Morgane</creator>
<creator>Gallais, Isabelle</creator>
<creator>Mograbi, Baharia</creator>
<creator>Podechard, Normand</creator>
<creator>Le Ferrec, Eric</creator>
<creator>Grova, Nathalie</creator>
<creator>Appenzeller, Brice</creator>
<creator>Burel, Agnès</creator>
<creator>Chevanne, Martine</creator>
<creator>Sergent, Odile</creator>
<creator>Huc, Laurence</creator>
<creator>Bortoli, Sylvie</creator>
<creator>Lagadic-Gossmann, Dominique</creator>
<contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Institut de Recherche sur le Cancer et le Vieillissement (IRCAN) ; Centre National de la Recherche Scientifique (CNRS) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Université Nice Sophia Antipolis (UNS) ; Université Côte d'Azur (UCA) - Université Côte d'Azur (UCA)</contributor>
<contributor>Laboratory of Analytical Human Biomonitoring-CRP-Santé ; Luxembourg Institute of Health</contributor>
<contributor>Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>ToxAlim (ToxAlim) ; Institut National Polytechnique [Toulouse] (INP) - Institut National de la Recherche Agronomique (INRA) - Université Paul Sabatier - Toulouse 3 (UPS) - Ecole Nationale Vétérinaire de Toulouse</contributor>
<contributor>Toxicologie, Pharmacologie et Signalisation Cellulaire (U1124) ; Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS)</contributor>
<contributor>Ligue Contre le Cancer (committees 22,35,49,85; DLG, OS), the French National Academy of Medicine (DLG), ANR (STEATOX project; “ANR-13-CESA-0009”; DLG, OS, BM), the ITMO-cancer Plan Cancer 2009–2013 (SB), “Region Provence Alpes Côte d’Azur”, “Agence régionale santé Provence Alpes Côte d’Azur”, “Direction régionale de l’Environnement, de l’aménagement et du logement Provence Alpes Côte d’Azur” (BM, plan régional santé environnement PRSE PACA n°6.3.3.3 and 6.3.3.4)</contributor>
<description>International audience</description>
<source>ISSN: 2045-2322</source>
<source>EISSN: 2045-2322</source>
<source>Scientific Reports</source>
<publisher>Nature Publishing Group</publisher>
<identifier>hal-01518808</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01518808</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01518808/document</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01518808/file/Hardonni%C3%A8re%20et%20al%202017.pdf</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01518808</source>
<source>Scientific Reports, Nature Publishing Group, 2017, 7 (1), pp.195. 〈10.1038/s41598-017-00269-7〉</source>
<identifier>DOI : 10.1038/s41598-017-00269-7</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1038/s41598-017-00269-7</relation>
<identifier>PUBMED : 28298645</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/28298645</relation>
<language>en</language>
<subject lang=en>Cancer metabolism</subject>
<subject lang=en>Predictive markers</subject>
<subject>[SDV.CAN] Life Sciences [q-bio]/Cancer</subject>
<subject>[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN]</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Most tumors undergo metabolic reprogramming towards glycolysis, the so-called Warburg effect, to support growth and survival. Overexpression of IF1, the physiological inhibitor of the F0F1ATPase, has been related to this phenomenon and appears to be a relevant marker in cancer. Environmental contributions to cancer development are now widely accepted but little is known about the underlying intracellular mechanisms. Among the environmental pollutants humans are commonly exposed to, benzo[a]pyrene (B[a]P), the prototype molecule of polycyclic aromatic hydrocarbons (PAHs), is a well-known human carcinogen. Besides apoptotic signals, B[a]P can also induce survival signals in liver cells, both likely involved in cancer promotion. Our previous works showed that B[a]P elicited a Warburg-like effect, thus favoring cell survival. The present study aimed at further elucidating the molecular mechanisms involved in the B[a]P-induced metabolic reprogramming, by testing the possible involvement of IF1. We presently demonstrate, both in vitro and in vivo, that PAHs, especially B[a]P, strongly increase IF1 expression. Such an increase, which might rely on β2-adrenergic receptor activation, notably participates to the B[a]P-induced glycolytic shift and cell survival in liver cells. By identifying IF1 as a target of PAHs, this study provides new insights about how environmental factors may contribute to related carcinogenesis.</description>
<date>2017</date>
<contributor>ANR-13-CESA-0009, STEATOX, Impact des agents chimiques environnementaux sur les mécanismes de progression pathologique de la stéatose hépatique(2013)</contributor>
</dc>
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