Journal
CELL METABOLISM
Volume 28, Issue 5, Pages 706-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2018.07.021
Keywords
-
Categories
Funding
- Austrian Science Fund FWF SFB LIPTOX [F3018, P27108, P28854, W1226 DK]
- Integrative Metabolism Research Center Graz
- Austrian infrastructure program 2016/2017
- Lustgarten Foundation
- SU2C
- Ludwig Center at MIT
- NCI [P30 CA1405141, R01 CA168653]
- Austrian Marshall Plan Scholarship
- Ludwig Center for Molecular Oncology Fund, NSF [GRFP DGE-1122374, T32GM007287]
- Damon Runyon Cancer Research Foundation [DRG-2241-15]
- CBmed - Center for Biomarker Research in Medicine
- NAWI Graz
- MIT Center for Precision Cancer Medicine
- Austrian Science Fund (FWF) [P27108, P28854] Funding Source: Austrian Science Fund (FWF)
Ask authors/readers for more resources
Mitochondrial function is important for aspartate biosynthesis in proliferating cells. Here, we show that mitochondrial aspartate export via the aspartate-glutamate carrier 1 (AGC1) supports cell proliferation and cellular redox homeostasis. Insufficient cytosolic aspartate delivery leads to cell death when TCA cycle carbon is reduced following glutamine withdrawal and/or glutaminase inhibition. Moreover, loss of AGC1 reduces allograft tumor growth that is further compromised by treatment with the glutaminase inhibitor CB-839. Together, these findings argue that mitochondrial aspartate export sustains cell survival in low-glutamine environments and AGC1 inhibition can synergize with glutaminase inhibition to limit tumor growth.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available