ArticleACS medicinal chemistry letters2015
Suppression of Hepatocellular Carcinoma by Inhibition of Overexpressed Ornithine Aminotransferase.
Article in ACS medicinal chemistry letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 49 citations in OpenAlex.
- Review
- Targeting Conformational Flexibility of a Reactive Intermediate to Enhance Selectivity of a GABA Aminotransferase Inactivator.Journal of the American Chemical Society · 2026Article
- Inactivation of ornithine aminotransferase by (1Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Article
- Beyond Ornithine Metabolism in Gyrate Atrophy: Tissue-Specific Proteomic Insights into Neonatal and Adult OAT Deficiency.bioRxiv : the preprint server for biology · 2025Article
- Construction of mitochondrial signature (MS) for the prognosis of ovarian cancer.Discover oncology · 2025Article
- RNA-Seq transcriptome profiling of Nile rat livers reveals novel insights on the anti-diabetic mechanisms of Water-Soluble Palm Fruit Extract.Journal of applied genetics · 2024Article
- Synthesis of (2The Journal of organic chemistry · 2024Article
- Design, Synthesis, and Mechanistic Studies of (ACS chemical biology · 2024Article
- Role of lung ornithine aminotransferase in idiopathic pulmonary fibrosis: regulation of mitochondrial ROS generation and TGF-β1 activity.Experimental & molecular medicine · 2024Article
- FromiScience · 2024Article
- Identification of Protein Targets ofACS chemical biology · 2024Article
- Dietary Manipulation of Amino Acids for Cancer Therapy.Nutrients · 2023Review
- Liver-directed gene therapy for ornithine aminotransferase deficiency.EMBO molecular medicine · 2023Article
- Article
- Structural and Mechanistic Basis for the Inactivation of Human Ornithine Aminotransferase by (3Molecules (Basel, Switzerland) · 2023Article
- Advancements in Hepatocellular Carcinoma: Potential Preclinical Drugs and their Future.Current pharmaceutical design · 2023Review
- Ornithine aminotransferase and carbamoyl phosphate synthetase 1 involved in ammonia metabolism serve as novel targets for early stages of gastric cancer.Journal of clinical laboratory analysis · 2022Article
- Determination of the pH dependence, substrate specificity, and turnovers of alternative substrates for human ornithine aminotransferase.The Journal of biological chemistry · 2022Article
- Rational Design, Synthesis, and Mechanism of (3Journal of the American Chemical Society · 2022Article
- Inactivators of Ornithine Aminotransferase for the Treatment of Hepatocellular Carcinoma.ACS medicinal chemistry letters · 2022Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma is the second leading cause of cancer death worldwide. DNA microarray analysis identified the ornithine aminotransferase (OAT) gene as a prominent gene overexpressed in hepatocellular carcinoma (HCC) from Psammomys obesus. In vitro studies demonstrated inactivation of OAT by gabaculine (1), a neurotoxic natural product, which suppressed in vitro proliferation of two HCC cell lines. Alpha-fetoprotein (AFP) secretion, a biomarker for HCC, was suppressed by gabaculine in both cell lines, but not significantly. Because of the active site similarity between GABA aminotransferase (GABA-AT) and OAT, a library of 24 GABA-AT inhibitors was screened to identify a more selective inhibitor of OAT. (1S,3S)-3-Amino-4-(hexafluoropropan-2-ylidene)cyclopentane-1-carboxylic acid (2) was found to be an inactivator of OAT that only weakly inhibits GABA-AT, l-aspartate aminotransferase, and l-alanine aminotransferase. In vitro administration of 2 significantly suppressed AFP secretion in both Hep3B and HepG2 HCC cells; in vivo, 2 significantly suppressed AFP serum levels and tumor growth in HCC-harboring mice, even at 0.1 mg/kg. Overexpression of the OAT gene in HCC and the ability to block the growth of HCC by OAT inhibitors support the role of OAT as a potential therapeutic target to inhibit HCC growth. This is the first demonstration of suppression of HCC by an OAT inactivator.
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