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* Inserm U602, Université Paris XI;
AP-HP, Hôpital Paul Brousse, Service de Biochimie et Biologie Moléculaire, Université Paris XI, Villejuif, France;
UMR 7091 CNRS, Université Paris VI, Génomique Fonctionnelle et Biologie des Systèmes pour la Santé, Villejuif, France;
AP-HP, Hôpital Ambroise Paré, Service d’Anatomie Pathologie, Université Versailles St. Quentin, Boulogne-Billancourt, France; and
|| Department of Research, Basel University Hospital, Basel, Switzerland
1Correspondence: Service de Biochimie et Biologie Moléculaire, Hôpital Universitaire Paul Brousse, Université Paris-Sud/XI, 14 Ave. Paul Vaillant Couturier, 94804 Villejuif Cedex, France. E-mail: antoinette.lemoine{at}pbr.ap-hop-paris.fr
Overexpression of T-cadherin (T-cad) transcripts occurs in 
50% of human hepatocellular carcinomas (HCCs). To elucidate T-cad functions in HCC, we examined T-cad protein expression in normal and tumoral human livers and hepatoma cell lines and investigated its influence on invasive potential of HCC using RNA interference silencing of T-cad expression in Mahlavu cells. Whereas T-cad expression was restricted to endothelial cells (EC) from large blood vessels in normal livers, it was up-regulated in sinusoidal EC from 8/15 invasive HCCs. Importantly, in three of them (38%) T-cad was detected in tumor cells within regions in which E-cadherin expression was absent. Among six hepatoma cell lines, only Mahlavu expressed T-cad but not E-cadherin. T-cad exhibited a globally punctuate distribution in quiescent Mahlavu and additionally it concentrated at the leading edge of migrating cells. Matrigel invasion assay revealed that Mahlavu possess a high invasive potential that was significantly inhibited by T-cad silencing. Wound healing and random motility assays demonstrated that inhibition of T-cad expression in Mahlavu significantly reduced their motility. We propose that T-cad expression in tumor cells might occur by cadherin-switching during epithelial-mesenchymal transition and may represent an additional mechanism contributing to HCC metastasis.—Riou, P., Saffroy, R., Chenailler, C., Franc, B., Gentile, C., Rubinstein, E., Resink, T., Debuire, B., Piatier-Tonneau, D., Lemoine, A. Expression of T-cadherin in tumor cells influences invasive potential of human hepatocellular carcinoma.
Key Words: primary tumors • cadherin switch • cell invasion • hepatoma cell lines • RNA interference
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