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<dc:title xml:lang="en">Mechanisms of Tenascin-C dependent tumor migration and metastasis</dc:title>
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<dc:subject xml:lang="fr">Ténascine-C</dc:subject>
<dc:subject xml:lang="fr">Cancer</dc:subject>
<dc:subject xml:lang="fr">Cellules tumorales disséminées</dc:subject>
<dc:subject xml:lang="fr">Lymphovasculaire invasion</dc:subject>
<dc:subject xml:lang="fr">EMT</dc:subject>
<dc:subject xml:lang="fr">Amiboïde migration</dc:subject>
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<dc:subject xml:lang="fr">TGF- β</dc:subject>
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<dc:subject xml:lang="en">Tenascin-C</dc:subject>
<dc:subject xml:lang="en">Cancer</dc:subject>
<dc:subject xml:lang="en">Circulating tumor cell</dc:subject>
<dc:subject xml:lang="en">Lymphovascular invasion</dc:subject>
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<dc:subject xml:lang="en">Amoeboid migration</dc:subject>
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<dcterms:abstract xml:lang="fr">Les métastases sont la principale cause de décès chez les patients atteints d’un cancer. Lors du développement métastatique, les cellules tumorales disséminées (CTD) doivent franchir certaines étapes clés avant de coloniser des organes distants de la tumeur primaire. Notre hypothèse est que la TNC pourrait jouer différents rôles dans la migration des cellules cancéreuses et par conséquent dans le développement métastatique. Considérant l’actine comme un réservoir de facteurs de croissance, la TNC pourrait induire la TEM ainsi que la survie et l’extravasation des cellules tumorales. Cependant, des cellules cancéreuses individualisées localement pourraient répondre à la TNC en initiant des changements rapides menant à un phénotype migratoire de type amiboïde. L’objectif de cette thèse a été d’étudier comment la TNC stimule le développement métastatique dans le cancer du sein au niveau cellulaire et moléculaire en utilisant des modèles tumoraux et cellulaires.</dcterms:abstract>
<dcterms:abstract xml:lang="en">A high TNC expression correlates with lung metastagenicity and was shown to promote experimental lung metastasis, but the underlying mechanisms are poorly understood. The results of my thesis have provided insight into the roles of TNC in metastasis suggesting that TNC contributes to extravasation by impacting on survival, endothelialization, EMT and migration. Moreover, I have identified TGF-β signaling and integrin α9β1 as important pathway and molecule, respectively to be employed by TNC. Whether both molecule/pathway play a similar role in the investigated models of breast cancer, osteosarcoma and glioblastoma remains to be seen.</dcterms:abstract>
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