原创力文档rad001 enhances the potency of bez235 to inhibit mtor signaling and tumor growthrad001增强的效力bez235抑制mtor信号和肿瘤的生长.pdfVIP
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rad001 enhances the potency of bez235 to inhibit mtor signaling and tumor growthrad001增强的效力bez235抑制mtor信号和肿瘤的生长
RAD001 Enhances the Potency of BEZ235 to Inhibit
mTOR Signaling and Tumor Growth
1 2 2 2 1 2
Beat Nyfeler , Yan Chen , Xiaoyan Li , Maria Pinzon-Ortiz , Zuncai Wang , Anupama Reddy ,
2 2 ´ 2 2 1 2
Elina Pradhan , Rita Das , Joseph Lehar , Robert Schlegel , Peter M. Finan , Z. Alexander Cao ,
1 2
Leon O. Murphy , Alan Huang *
1 Developmental and Molecular Pathways, Novartis Institutes for BioMedical Research, Cambridge, Massachusetts, United States of America, 2 Oncology Translational
Medicine, Novartis Institutes for BioMedical Research, Cambridge, Massachusetts, United States of America
Abstract
The mammalian target of rapamycin (mTOR) is regulated by oncogenic growth factor signals and plays a pivotal role in
controlling cellular metabolism, growth and survival. Everolimus (RAD001) is an allosteric mTOR inhibitor that has shown
marked efficacy in certain cancers but is unable to completely inhibit mTOR activity. ATP-competitive mTOR inhibitors such
as NVP-BEZ235 can block rapamycin-insensitive mTOR readouts and have entered clinical development as anti-cancer
agents. Here, we show the degree to which RAD001 and BEZ235 can be synergistically combined to inhibit mTOR pathway
activation, cell proliferation and tumor growth, both in vitro and in vivo. RAD001 and BEZ235 synergized in cancer lines
representing different lineages and genetic backgrounds. Strong synergy is seen in neuronal, renal, breast, lung, and
haematopoietic cancer cells harboring abnormalities in PTEN, VHL, LKB1, Her2, or KRAS. Critically, in the presence of
RAD0
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