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PI3-K/Akt pathway contributes to IL-6-dependent growth of 7TD1 cells

BACKGROUND: Recently, growing evidence suggests the involvement of PI 3-K/Akt in IL-6-dependent survival and proliferative responses in several types of cells. However, whether PI 3-K/Akt plays the same role in IL-6-dependent growth of 7TD1 mouse-mouse B cell hybridoma is not known. METHODS: We inve...

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Detalles Bibliográficos
Autores principales: Zhang, JiYan, Li, Yan, Shen, BeiFen
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2003
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC151674/
https://www.ncbi.nlm.nih.gov/pubmed/12633505
http://dx.doi.org/10.1186/1475-2867-3-1
Descripción
Sumario:BACKGROUND: Recently, growing evidence suggests the involvement of PI 3-K/Akt in IL-6-dependent survival and proliferative responses in several types of cells. However, whether PI 3-K/Akt plays the same role in IL-6-dependent growth of 7TD1 mouse-mouse B cell hybridoma is not known. METHODS: We investigated the activation status of Akt in 7TD1 cells induced by IL-6. With PI 3-K specific inhibitor wortmannin, we also investigated the biological roles of Akt activation in 7TD1 cells. RESULTS: IL-6 stimulated phosphorylation of Akt in a dose- and time-dependent manner in 7TD1 cells. Wortmannin significantly reduced IL-6-induced phosphorylation of Akt and IL-6-dependent growth of 7TD1 cells. Furthermore, wortmannin blocked IL-6-induced up-regulation of XIAP, but not Bcl-2 in 7TD1 cells. CONCLUSION: The data suggest that IL-6-induced PI 3-K/Akt activation is essential for the optimal growth of 7TD1 cells through up-regulation of anti-apoptosis proteins such as XIAP.