ArticleFrontiers in physiology2019
Liquiritin, as a Natural Inhibitor of AKR1C1, Could Interfere With the Progesterone Metabolism.
Article in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Role of Aldo-Keto reductase family 1 member C in cancer progression: a special focus on the role of AKR1C1 in pancreatic cancer.Medical oncology (Northwood, London, England) · 2025Article
- Comparative Analysis of Coumarin Profiles in Different Parts ofMolecules (Basel, Switzerland) · 2022Article
- Wen Dan Tang: A Potential Jing Fang Decoction for Headache Disorders?Medicines (Basel, Switzerland) · 2022Review
- AKR1C1 connects autophagy and oxidative stress by interacting with SQSTM1 in a catalytic-independent manner.Acta pharmacologica Sinica · 2022Article
- Analogues of Natural Chalcones as Efficient Inhibitors of AKR1C3.Metabolites · 2022Article
- Natural Product Alantolactone Targeting AKR1C1 Suppresses Cell Proliferation and Metastasis in Non-Small-Cell Lung Cancer.Frontiers in pharmacology · 2022Article
- The Interaction of lncRNA XLOC-2222497,International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Low progesterone level is always linked with pre-term birth. Therefore, maintaining of progesterone level is vital during pregnancy. Aldo-keto reductase family one member C1 (AKR1C1) catalyzes the reduction of progesterone to its inactive form of 20-alpha-hydroxy-progesterone and thus limits the biological effect of progesterone. In our effort to identify the natural compound that would specifically inhibit AKR1C1, liquiritin was found to be a selective and potent inhibitor of AKR1C1. Kinetic analyses in the S-(+)-1,2,3,4-tetrahydro-1-naphthol (s-tetralol) catalyzed by AKR1C1 in the presence of the inhibitors suggest that liquiritin is a competitive inhibitor by targeting the residues Ala-27, Val-29, Ala-25, and Asn-56 of AKR1C1. In HEC-1-B cells, treatment with liquiritin results in 85.00% of reduction in progesterone metabolism, which is mediated by AKR1C1 enzymatic activity. Overall, our study not only identify liquiritin as an inhibitor against AKR1C1, but also reveal that liquiritin may be served as a potential intervention strategy for preventing pre-term birth caused by low progesterone level.
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