Cited by 291Metabolism, Diabetes, and CancerPI3K/AKT/mTOR signaling in cancerCancer, Hypoxia, and Metabolism

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The AMPK Inhibitor Compound C Is a Potent AMPK-Independent Antiglioma Agent

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Liu, Xiaona, Chhipa, Rishi Raj, Nakano, Ichiro, Dasgupta, Biplab·2014·Molecular Cancer Therapeutics

DOI 10.1158/1535-7163.mct-13-0579PMC PMC3954437

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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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Authors: Liu, X., Chhipa, R. R., Nakano, I., & Dasgupta, B.
Affiliations: Cincinnati Children's Hospital Medical Center (US)
Corresponding author: Dasgupta, Biplab
ORCID: Liu, Xiaona
Chhipa, Rishi Raj
Nakano, Ichiro
Dasgupta, Biplab
Venue: Molecular Cancer Therapeutics
Publisher: American Association for Cancer Research (AACR)
Published: 2014-03-01
Volume: 13
Issue: 3
Pages: 596-605
ISSN: 1535-7163 (ISSN-L)
1538-8514
DOI: 10.1158/1535-7163.mct-13-0579
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

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The AMPK Inhibitor Compound C Is a Potent AMPK-Independent Antiglioma Agent

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