ArticleMedical oncology (Northwood, London, England)2025
αKG-induced oxidative stress and mTOR inhibition as a therapeutic strategy for liver cancer.
Article in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Crosstalk BetweenCancers · 2026Review
- Mitochondria: from powerhouses of cells to hubs in antitumor immunity.Frontiers in immunology · 2026Review
- Metabolic Signatures of Acinetobacter baumannii and Klebsiella pneumoniae Infections in Acute-on-chronic Liver Failure.Cellular and molecular gastroenterology and hepatology · 2026Article
- Mn-MIL-100@AKG alleviates intervertebral disc degeneration by regulating mitophagy.Materials today. Bio · 2025Article
- Molecular mechanisms and clinical significance of perineural invasion in malignancies: the pivotal role of tumor-associated Schwann cells in cancer progression and metastasis.Medical oncology (Northwood, London, England) · 2025Review
- Protective effects of α-ketoglutaric acid on palmitic acid-induced deterioration in sheep endometrial epithelial cells via ferroptosis inhibition.Frontiers in veterinary science · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Despite the availability of targeted therapies, liver cancer remains a severe health burden. The need for adjuvant therapy to improve treatment efficacy and prevent recurrence is emerging. Alpha-ketoglutarate (αKG) is an intermediate in the tricarboxylic acid cycle and a cofactor for various oxygenases. A critical role of this multifunctional metabolite has started to be revealed in physiological and pathological conditions. We found that αKG exerts various anti-tumor effects in liver cancer cells. Our kinetic transcriptome study suggested that increasing reactive oxygen species and inhibiting mTORC1 signaling underlies. Indeed, αKG treatment elevated oxidative stress and induced DNA damage, presumably caused by early downregulation of the antioxidant gene SLC7A11. Further, we validated impaired mTOR signaling and decreased cellular energy production. This unique mechanism underscores αKG's potential as a liver cancer therapy by harnessing oxidative stress and disrupting metabolic signaling. These findings could provide valuable insights into further exploration of αKG as a promising therapeutic agent in liver cancer.
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