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AB98. The study of cell proliferation and apoptosis and autophagy in renal cell carcinoma cells influence by the PI3K/AKT/mTor inhibitor NVP-BEZ235

OBJECTIVE: The research is to study the cell proliferation and apoptosis and autophagy in renal cell carcinoma cells influence by the PI3K/AKT/mTor inhibitor NVP-BEZ235. Looking for a new treatment strategy of renal cell carcinoma. METHODS: we test the effect of NVP on survival rate, apoptosis and a...

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Detalles Bibliográficos
Autores principales: Li, Hong-Yan, Han, Yu-Ping, Jin, Xue-Fei, Xing, Yuan-Yuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4708368/
http://dx.doi.org/10.3978/j.issn.2223-4683.2014.s098
Descripción
Sumario:OBJECTIVE: The research is to study the cell proliferation and apoptosis and autophagy in renal cell carcinoma cells influence by the PI3K/AKT/mTor inhibitor NVP-BEZ235. Looking for a new treatment strategy of renal cell carcinoma. METHODS: we test the effect of NVP on survival rate, apoptosis and autophagy in the RCC cell line, 786-0. We also explore the hypothesis that NVP, in combination with autophagy inhibitors, leads to apoptosis enhancement in 786-0 cells. RESULTS: the PI3K/AKT/mTOR pathway proteins p-AKT and p-P70S6K were highly expressed in RCC tissue. We also showed that NVP inhibited cell growth and induced apoptosis and autophagy in RCC cells. The combination treatment of NVP with autophagy inhibitors enhanced the effect of NVP on suppressing 786-0 growth and induction of apoptosis. CONCLUSIONS: PI3K/AKT/mTOR signaling pathways protein in renal cell carcinoma tissues expression levels; PI3K/mTOR inhibitor NVP-BEZ235 can significantly inhibit renal cell 786-0 cell proliferation and promote the occurrence of apoptosis; Autophagy inhibitor can significantly improve the NVP-BEZ235 cause 786-0 proliferation inhibition and apoptosis.