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. Author manuscript; available in PMC: 2017 Jul 7.
Published in final edited form as: Bioessays. 2016 Jul 18;38(9):839–844. doi: 10.1002/bies.201600026

Figure 2.

Figure 2

Extracellular nutrients are required to maintain growth factor receptor signaling through mTORC2.

mTORC2 forms an auto-activation loop (i) by promoting glucose/acetate uptake and acetyl-CoA production through its downstream pathways of c-Myc [11] and (ii) by an activation of mTORC2 through acetyl-CoA-dependent acetylation of Rictor [36]. By these mechanisms, GBM cells with activated mTORC2 are resistant to molecularly targeted therapies toward their upstream stimulators, including EGFR. This study suggests that altered cellular metabolism is not only a consequence of oncogenic signaling, but also an important determinant of its activity, raising the possibility that systemic metabolism may contribute to resistance to targeted cancer therapies [59]. Ac, acetyl-group; Ac-CoA, acetyl-CoA.