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The AMPK Inhibitor Compound C Is a Potent AMPK-Independent Antiglioma Agent
Open accessPublished version of a preprint
Abstract
AMP-activated protein kinase (AMPK) is an evolutionarily conserved energy sensor important for cell growth, proliferation, survival, and metabolic regulation. Active AMPK inhibits biosynthetic enzymes like mTOR and acetyl CoA carboxylase (required for protein and lipid synthesis, respectively) to ensure that cells maintain essential nutrients and energy during metabolic crisis. Despite our knowledge about this incredibly important kinase, no specific chemical inhibitors are available to examine its function. However, one small molecule known as compound C (also called dorsomorphin) has been widely used in cell-based, biochemical, and in vivo assays as a selective AMPK inhibitor. In nearly all these reports including a recent study in glioma, the biochemical and cellular effects of compound C have been attributed to its inhibitory action toward AMPK. While examining the status of AMPK activation in human gliomas, we observed that glioblastomas express copious amount of active AMPK. Compound C effectively reduced glioma viability in vitro both by inhibiting proliferation and inducing cell death. As expected, compound C inhibited AMPK; however, all the antiproliferative effects of this compound were AMPK independent. Instead, compound C killed glioma cells by multiple mechanisms, including activation of the calpain/cathepsin pathway, inhibition of AKT, mTORC1/C2, cell-cycle block at G2–M, and induction of necroptosis and autophagy. Importantly, normal astrocytes were significantly less susceptible to compound C. In summary, compound C is an extremely potent antiglioma agent but we suggest that caution should be taken in interpreting results when this compound is used as an AMPK inhibitor. Mol Cancer Ther; 13(3); 596–605. ©2014 AACR.
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Metadata
- Authors
- Liu, X., Chhipa, R. R., Nakano, I., & Dasgupta, B.
- Affiliations
- Cincinnati Children's Hospital Medical Center (US)
- Corresponding author
- Dasgupta, Biplab
- Venue
- Molecular Cancer Therapeutics
- Published
- 2014-03-01
- Volume
- 13
- Issue
- 3
- Pages
- 596-605
- ISSN
- 1535-7163 (ISSN-L)
- 1538-8514
- PMC
- PMC3954437
- OpenAlex
- W2104267594
- Cited by
- 288
- References
- 42
- Citations by year
- 2026: 21 · 2025: 18 · 2024: 17 · 2023: 24 · 2022: 23 · 2021: 31 · 2020: 23 · 2019: 27 · 2018: 27 · 2017: 28 · 2016: 23 · 2015: 16 · 2014: 10
- FWCI
- 10.52
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Cancer Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS075291)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Keywords
- compound C, AMPK, glioma, glioblastoma, AKT inhibition, mTOR inhibition, G2/M cell cycle arrest, necroptosis, autophagy, astrocytes, antiproliferative activity
- MeSH terms
- Brain Neoplasms, Glioma, Humans, Pyrazoles, Pyrimidines, Apoptosis, Cell Line, Tumor, Protein Kinase Inhibitors, Cell Proliferation, AMP-Activated Protein Kinases, TOR Serine-Threonine Kinases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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