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<title lang=en>Aryl hydrocarbon receptor-dependent up-regulation of the heterodimeric amino acid transporter LAT1 (SLC7A5)/CD98hc (SLC3A2) by diesel exhaust particle extract in human bronchial epithelial cells</title>
<creator>Le Vee, Marc</creator>
<creator>Jouan, Elodie</creator>
<creator>Lecureur, Valérie</creator>
<creator>FARDEL, Olivier</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>CHU Pontchaillou [Rennes]</contributor>
<description>International audience</description>
<source>ISSN: 0041-008X</source>
<source>EISSN: 1096-0333</source>
<source>Toxicology and Applied Pharmacology</source>
<publisher>Elsevier</publisher>
<identifier>hal-01237095</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01237095</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01237095/document</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01237095/file/Aryl%20hydrocarbon%20receptor-dependent%20up-regulation_accepted.pdf</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01237095</source>
<source>Toxicology and Applied Pharmacology, Elsevier, 2016, 290, pp.74-85. 〈10.1016/j.taap.2015.11.014〉</source>
<identifier>DOI : 10.1016/j.taap.2015.11.014</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.taap.2015.11.014</relation>
<identifier>PUBMED : 26621329</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/26621329</relation>
<language>en</language>
<subject lang=en>Lung</subject>
<subject lang=en>leucin</subject>
<subject lang=en>amino acid transporter</subject>
<subject lang=en>Aryl hydrocarbon receptor</subject>
<subject lang=en>diesel exhaust particle</subject>
<subject lang=en>matrix metalloproteinase-2</subject>
<subject>[SDV] Life Sciences [q-bio]</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>The heterodimeric L-type amino acid transporter (LAT) 1/ CD98hc is overexpressed in lung cancers with a poor prognosis factor. Factors that contribute to LAT1/CD98hc overexpression in lung cells remain however to be determined, but the implication of atmospheric pollution can be suspected. The present study was therefore designed to analyze the effects of diesel exhaust particle (DEP) extract (DEPe) on LAT1/CD98hc expression in bronchial epithelial BEAS-2B cells. Exposure to DEPe up-regulated LAT1 and CD98hc mRNA levels in a concentration-dependent manner, with DEPe EC50 values (around 0.2 μg/mL) relevant to environmental situations. DEPe concomitantly induced LAT1/CD98hc protein expression and LAT1-mediated leucine accumulation in BEAS-2B cells. Inhibition of the aryl hydrocarbon receptor (AhR) pathway through the use of a chemical AhR antagonist or the siRNA-mediated silencing of AhR expression was next found to prevent DEPe-mediated induction of LAT1/CD98hc, indicating that this regulation depends on AhR, known to be activated by major chemical DEP components like polycyclic aromatic hydrocarbons. DEPe exposure was finally shown to induce mRNA expression and activity of matrix metalloproteinase (MMP)-2 in BEAS-2B cells, in a CD98hc/focal adhesion kinase (FAK)/extracellular regulated kinase (ERK) manner, thus suggesting that DEPe-mediated induction of CD98hc triggers activation of the integrin/FAK/ERK signaling pathway known to be involved in MMP-2 regulation. Taken together, these data demonstrate that exposure to DEPe induces functional overexpression of the amino acid transporter LAT1/CD98h in lung cells. Such a regulation may participate to pulmonary carcinogenic effects of DEPs, owing to the well-documented contribution of LAT1 and CD98hc to cancer development.</description>
<date>2016-01-01</date>
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