A Kinase Inhibitor Targeted to mTORC1 Drives Regression in Glioblastoma.
A Kinase Inhibitor Targeted to mTORC1 Drives Regression in Glioblastoma.
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DOI:
10.1016/j.ccell.2017.01.014
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发表时间:
2017-03-13
期刊:
影响因子:
50.3
通讯作者:
Weiss WA
中科院分区:
文献类型:
--
作者:
Fan Q;Aksoy O;Wong RA;Ilkhanizadeh S;Novotny CJ;Gustafson WC;Truong AY;Cayanan G;Simonds EF;Haas-Kogan D;Phillips JJ;Nicolaides T;Okaniwa M;Shokat KM;Weiss WA
Although signaling from PI3K and AKT to mTOR is prominently dysregulated in high-grade glial brain tumors, blockade of PI3K or AKT minimally affects downstream mTOR activity in glioma. Allosteric mTOR inhibitors, such as rapamycin, incompletely block mTORC1 compared to mTOR kinase inhibitors (TORKi). Here, we compared RapaLink-1, a TORKi linked to rapamycin, with earlier generation mTOR inhibitors. Compared to rapamycin and Rapalink-1, TORKi showed poor durability. RapaLink-1 associated with FKBP12, an abundant mTOR-interacting protein, enabling accumulation of RapaLink-1. RapaLink-1 showed better efficacy than rapamycin or TORKi, potently blocking cancer-derived, activating mutants of mTOR. Our study re-establishes mTOR as a central target in glioma and traces the failure of existing drugs to incomplete/nondurable inhibition of mTORC1. Fan et al. target mTORC1 activity in glioblastoma (GBM) with RapaLink-1, which is comprised of rapamycin linked to an mTOR kinase inhibitor. RapaLink-1 decreases mTORC1 activity in the brain and suppresses the growth of GBM xenografts and a genetically-engineered mouse model of brain cancer in vivo.