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Cancer Biol Med. 2014 Dec;11(4):255-63. doi: 10.7497/j.issn.2095-3941.2014.04.004.

Emerging function of mTORC2 as a core regulator in glioblastoma: metabolic reprogramming and drug resistance.

Author information

1
1 Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, CA 92093, USA ; 2 Neuro-Oncology Program, University of California, Los Angeles, CA 90095, USA.

Abstract

Glioblastoma (GBM) is one of the most lethal human cancers. Genomic analyses define the molecular architecture of GBM and highlight a central function for mechanistic target of rapamycin (mTOR) signaling. mTOR kinase exists in two multi-protein complexes, namely, mTORC1 and mTORC2. These complexes differ in terms of function, regulation and rapamycin sensitivity. mTORC1 is well established as a cancer drug target, whereas the functions of mTORC2 in cancer, including GBM, remains poorly understood. This study reviews the recent findings that demonstrate a central function of mTORC2 in regulating tumor growth, metabolic reprogramming, and targeted therapy resistance in GBM, which makes mTORC2 as a critical GBM drug target.

KEYWORDS:

Glioblastoma; PI3K; Warburg effect; mTOR; mTORC2; metabolic reprogramming

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