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

• 作 者: Si-Han Wu Jun-Feng Bi Timothy Cloughesy Webster K.Cavenee Paul S.Mischel
• 机 构: Ludwig Institute for Cancer Research, University of California,Neuro-Oncology Program,University of
• 出 处: Cancer Biology & Medicine
• 发表日期: 2014年04期
• 关键词: rapamycin regulator understood complexes highlight targeted poorly regulating me

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(m TOR) signaling. m TOR kinase exists in two multiprotein complexes, namely, m TORC1 and m TORC2. These complexes differ in terms of function, regulation and rapamycin sensitivity. m TORC1 is well established as a cancer drug target, whereas the functions of m TORC2 in cancer, including GBM, remains poorly understood. This study reviews the recent findings that demonstrate a central function of m TORC2 in regulating tumor growth, metabolic reprogramming, and targeted therapy resistance in GBM, which makes m TORC2 as a critical GBM drug target.

Glioblastoma (GBM) is one of the most lethal human cancers. Genomic analyzes define the molecular architecture of GBM and highlight a central function for mechanistic target of rapamycin (mTOR) signaling. M TOR kinase exists in two multiprotein complexes, namely, m TORC1 and m TORC2. These complexes differ in terms of function, regulation and rapamycin sensitivity. m TORC1 is well established as a cancer drug target, while the functions of m TORC2 in cancer, including GBM, remains poorly understood. that demonstrated a central function of m TORC2 in regulating tumor growth, metabolic reprogramming, and targeted therapy resistance in GBM, which makes m TORC2 as a critical GBM drug target.