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<title lang=en>MEK/ERK-dependent uPAR expression is required for motility via phosphorylation of P70S6K in human hepatocarcinoma cells.</title>
<creator>Bessard, Anne</creator>
<creator>Frémin, Christophe</creator>
<creator>Ezan, Frédéric</creator>
<creator>Coutant, Alexandre</creator>
<creator>Baffet, Georges</creator>
<contributor>Signalisation et Réponses aux Agents Infectieux et Chimiques (SeRAIC) ; Université de Rennes 1 (UR1) - IFR140</contributor>
<contributor>Régulations des équilibres fonctionnels du foie normal et pathologique ; Université de Rennes 1 (UR1) - IFR140 - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<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>
<description>International audience</description>
<source>ISSN: 0021-9541</source>
<source>EISSN: 1097-4652</source>
<source>Journal of Cellular Physiology</source>
<publisher>Wiley</publisher>
<identifier>hal-00697044</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-00697044</identifier>
<source>https://hal.archives-ouvertes.fr/hal-00697044</source>
<source>Journal of Cellular Physiology, Wiley, 2007, 212 (2), pp.526-36. 〈10.1002/jcp.21049〉</source>
<identifier>DOI : 10.1002/jcp.21049</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1002/jcp.21049</relation>
<identifier>PUBMED : 17427199</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/17427199</relation>
<language>en</language>
<subject>[SDV.BC] Life Sciences [q-bio]/Cellular Biology</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Motility and invasiveness events require specific intracellular signaling cascade activations. In cancer liver cells, one of these mechanisms could involve the MAPK MEK/ERK cascade activation which has been shown over expressed and activated in hepatocellular carcinoma. To study whether the MEK/ERK cascade is involved in the motility of HCC, we examined the effect of MEK inhibitor and ERK2 silencing using monolayer wound-healing assays and fluoroblock invasion systems. Evidence was provided that the MAPK cascade is a key transduction pathway which controls HCC cells motility and invasiveness. We could disconnect proliferation to motility using mitomycin C and we established that RNAi-mediated inhibition of ERK2 led to strongly reduced cell motility. To improve our understanding, we analysed the regulation and the role of urokinase receptor (uPAR) in this process. We provided evidence that uPAR was under a MEK/ERK dependent mechanism and blocking uPAR activity using specific antagonist or inhibiting its expression by RNA interference which resulted in complete inhibition of motility. Moreover, we found in MAPK inhibited cultures and in uPAR silencing cells that p70S6K phosphorylation on residue Thr-389 was significantly reduced, whereas Ser-421/Thr-424 phosphorylation did not change. We highlighted that the FRAP/mTOR pathway did not affect motility and Thr-389 phosphorylation. Furthermore, we demonstrated that p70S6K inhibition by RNA interference completely inhibited hepatocarcinoma cell motility. Therefore, targeting uPAR and/or MEK/ERK/S6K by RNA interference could be a major therapeutic strategy for the future treatment of invasive hepatocarcinoma cells.</description>
<date>2007-08</date>
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