Synthetic lethality in KRas-driven cancer cells created by glutamine deprivation
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deaminated to glutamate by glutaminase (GLS).Glutamate is then converted to α-ketoglutarate by glutamate oxaloacetate transaminase (GOT).Aminooxyacetate (AOA) inhibits GOT and therefore suppresses generation of α-ketoglutarate from Gln-derived glutamate.The aspartate generated by GOT is critical for nucleotide and amino acid biosynthesis.B. The relative positions of the growth factor-dependent Restriction Point and late G 1 metabolic checkpoints mediated by essential amino acids (EAA), Gln and mTOR are depicted.
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KRAS-dependent upregulation of GOT1/2 in pancreatic cancer facilitates aspartate production for nucleotide biosynthesis and allows NADPH generation via ME1.
“For instance, KRAS-dependent upregulation of Glutamate Oxaloacetate Transaminase 1,2. (GOT) expression in pancreatic cancer facilitates production of aspartate for nucleotide biosynthesis, and allows NADPH generation via ME157,58 (Fig 2).”
From The metabolic landscape of RAS-driven cancers from biology to therapy (2021) · cites this paper as [58]
Limiting glutamine use combined with chemotherapy halts pancreatic tumor growth in preclinical mouse models and is not toxic to normal cells.
“Limiting glutamine use combined with chemotherapy is a viable means to halt pancreatic tumor growth in preclinical mouse models and is not toxic to normal cells58,60,65.”
From The metabolic landscape of RAS-driven cancers from biology to therapy (2021) · cites this paper as [58]
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References 8 · Cited by 61
- Authors
- Mukhopadhyay, S., Saqcena, M., & Foster, D. A.
- Affiliations
- Hunter College (US)
- City University of New York (US)
- Corresponding author
- Foster, David A.
- Venue
- Oncoscience
- Publisher
- Impact Journals, LLC
- Published
- 2015-09-23
- Volume
- 2
- Issue
- 10
- Pages
- 807-808
- ISSN
- 2331-4737 (ISSN-L)
- PMC
- PMC4671930
- OpenAlex
- W2415181728
- Cited by
- 61
- References
- 8
- Citations by year
- 2025: 1 · 2024: 5 · 2023: 3 · 2022: 8 · 2021: 21 · 2020: 9 · 2019: 11 · 2018: 3
- FWCI
- 0.33
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Locations
- Oncoscience (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
- Keywords
- synthetic lethality, KRAS-driven cancers, glutamine deprivation, glutaminase, aspartate aminotransferase, aminooxyacetic acid, alpha-ketoglutarate, aspartate biosynthesis, essential amino acids, mTOR, restriction point
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