PT  - JOURNAL ARTICLE
AU  - Si-Han Wu
AU  - Jun-Feng Bi
AU  - Timothy Cloughesy
AU  - Webster K. Cavenee
AU  - Paul S. Mischel
TI  - Emerging function of mTORC2 as a core regulator in glioblastoma: metabolic reprogramming and drug resistance
AID  - 10.7497/j.issn.2095-3941.2014.04.004
DP  - 2014 Dec 01
TA  - Cancer Biology and Medicine
PG  - 255--263
VI  - 11
IP  - 4
4099  - http://www.cancerbiomed.org/content/11/4/255.short
4100  - http://www.cancerbiomed.org/content/11/4/255.full
SO  - Cancer Biol Med2014 Dec 01; 11
AB  - 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.