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

Si-Han Wu; Jun-Feng Bi; Timothy Cloughesy; Webster K Cavenee; Paul S Mischel

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

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

Authors

Si-Han Wu¹, Jun-Feng Bi¹, Timothy Cloughesy¹, Webster K Cavenee¹, Paul S Mischel¹

Affiliation

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.

PMID: 25610711
PMCID: PMC4296088
DOI: 10.7497/j.issn.2095-3941.2014.04.004

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.

Publication types

Review

Abstract

Publication types

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