RIPK4 promoted the tumorigenicity of nasopharyngeal carcinoma cells - 13/11/18
pages | 6 |
Iconographies | 5 |
Vidéos | 0 |
Autres | 0 |
Highlights |
• | RIPK4 promoted the growth and anchorage-independent growth of NPC cells. |
• | RIPK4 promoted the expression of VEGF by activating NF-kB signaling. |
• | Axitinib showed therapeutic effects for NPC. |
Abstract |
RIPK4 (receptor interacting serine/threonine kinase 4) has been reported to be aberrantly expressed in several cancer types. However, its expression pattern and functions in nasopharyngeal carcinoma (NPC) have never been reported. In this study, we have shown that the expression of RIPK4 was up-regulated in NPC tissues. RIPK4 promoted the growth and anchorage-independent growth of NPC cells, and down-regulation of RIPK4 inhibited the growth of NPC cells both in the plate-based culture and on the soft agar. Moreover, RIPK4 promoted the expression of VEGF in the NPC cells and induced the tube formation of HUVEC, and Axitinib (the inhibitor for VEGF receptor) inhibited the tumorigenesis driven by RIPK4. In the molecular mechanism study, RIPK4 was found to enhance the interaction between IKKα and IKKβ, and activated NF-kB signaling. Taken together, our study demonstrated the oncogenic roles of RIPK4 in NPC and suggested that RIPK4 might be a therapeutic target.
Le texte complet de cet article est disponible en PDF.Keywords : RIPK4, NPC, VEGF, NF-kB signaling
Plan
Vol 108
P. 1-6 - décembre 2018 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
L’accès au texte intégral de cet article nécessite un abonnement.
Bienvenue sur EM-consulte, la référence des professionnels de santé.
L’achat d’article à l’unité est indisponible à l’heure actuelle.
Déjà abonné à cette revue ?