Oncogenic EGFR signaling activates an mTORC2-NF-κB pathway that promotes chemotherapy resistance

Although it is known that mTOR complex 2 (mTORC2) functions upstream of Akt, the role of this protein kinase complex in cancer is not well understood. Through an integrated analysis of cell lines, in vivo models, and clinical samples, we demonstrate that mTORC2 is frequently activated in glioblastom...

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Veröffentlicht in:	Cancer discovery 2011-11, Vol.1 (6), p.524-538
Hauptverfasser:	Tanaka, Kazuhiro, Babic, Ivan, Nathanson, David, Akhavan, David, Guo, Deliang, Gini, Beatrice, Dang, Julie, Zhu, Shaojun, Yang, Huijun, De Jesus, Jason, Amzajerdi, Ali Nael, Zhang, Yinan, Dibble, Christian C, Dan, Hancai, Rinkenbaugh, Amanda, Yong, William H, Vinters, Harry V, Gera, Joseph F, Cavenee, Webster K, Cloughesy, Timothy F, Manning, Brendan D, Baldwin, Albert S, Mischel, Paul S
Format:	Artikel
Sprache:	eng
Schlagworte:	Brain Neoplasms - drug therapy Brain Neoplasms - genetics Brain Neoplasms - metabolism Cell Line, Tumor Cell Survival - drug effects Cell Survival - physiology Cisplatin - pharmacology Drug Resistance, Neoplasm Glioblastoma - drug therapy Glioblastoma - genetics Glioblastoma - metabolism Humans NF-kappa B - genetics NF-kappa B - metabolism Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism PTEN Phosphohydrolase - genetics PTEN Phosphohydrolase - metabolism Receptor, Epidermal Growth Factor - genetics Receptor, Epidermal Growth Factor - metabolism Signal Transduction TOR Serine-Threonine Kinases - metabolism
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