ArticleThe Journal of steroid biochemistry and molecular biology2010
Aldo-keto reductase 1C3 expression in MCF-7 cells reveals roles in steroid hormone and prostaglandin metabolism that may explain its over-expression in breast cancer.
Article in The Journal of steroid biochemistry and molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 109 citations in OpenAlex.
- Environmental Lead Promotes Breast Cancer Migration and Invasion via the AKR1C3-NF-κB-MMP Axis.Biomedicines · 2026Article
- GWAS-based polygenic profiling across broad sport categories: shared and category-specific genetic associations with athlete status and polygenic differences from population controls.Frontiers in sports and active living · 2026Article
- 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
- Deciphering 17-β-hydroxysteroid dehydrogenase 4: from molecular insights to cancer therapeutics.Cancer cell international · 2025Review
- Analysis of Expression and Regulation of AKR1C2 in HPV-Positive and -Negative Oropharyngeal Squamous Cell Carcinoma.Cancers · 2024Article
- Aldo-keto reductase (AKR) superfamily website and database: An update.Chemico-biological interactions · 2024Article
- Design and Evaluation of NSAID Derivatives as AKR1C3 Inhibitors for Breast Cancer Treatment through Computer-Aided Drug Design and In Vitro Analysis.Molecules (Basel, Switzerland) · 2024Article
- AKR1C3 in carcinomas: from multifaceted roles to therapeutic strategies.Frontiers in pharmacology · 2024Review
- Aldo-keto reductases: Role in cancer development and theranostics.Oncology research · 2024Review
- Genetic association study of Preterm birth and Gestational age in a population-based case-control study in Peru: Genetics of PTB and GA in pregnant women in Peru.medRxiv : the preprint server for health sciences · 2023Article
- Isocitrate dehydrogenase 2 inhibitor enasidenib synergizes daunorubicin cytotoxicity by targeting aldo-keto reductase 1C3 and ATP-binding cassette transporters.Archives of toxicology · 2022Article
- Bruton's Tyrosine Kinase Inhibitor Zanubrutinib Effectively Modulates Cancer Resistance by Inhibiting Anthracycline Metabolism and Efflux.Pharmaceutics · 2022Article
- Characterization of the major single nucleotide polymorphic variants of aldo-keto reductase 1C3 (type 5 17β-hydroxysteroid dehydrogenase).The Journal of steroid biochemistry and molecular biology · 2022Article
- Analogues of Natural Chalcones as Efficient Inhibitors of AKR1C3.Metabolites · 2022Article
- Downregulation of Dihydrotestosterone and Estradiol Levels by HEXIM1.Endocrinology · 2022Article
- Aldo-Keto Reductases and Cancer Drug Resistance.Pharmacological reviews · 2021Review
- Deletion of Alox15 improves kidney dysfunction and inhibits fibrosis by increased PGDClinical and experimental nephrology · 2021Article
- Identification of significantly mutated subnetworks in the breast cancer genome.Scientific reports · 2021Article
- Selective inhibition of aldo-keto reductase 1C3: a novel mechanism involved in midostaurin and daunorubicin synergism.Archives of toxicology · 2021Article
- AKR1C3 Is Associated with Better Survival of Patients with Endometrial Carcinomas.Journal of clinical medicine · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Aldo-keto reductase (AKR) 1C3 (type 5 17beta-hydroxysteroid dehydrogenase and prostaglandin F synthase), may stimulate proliferation via steroid hormone and prostaglandin (PG) metabolism in the breast. Purified recombinant AKR1C3 reduces PGD(2) to 9alpha,11beta-PGF(2), Delta(4)-androstenedione to testosterone, progesterone to 20alpha-hydroxyprogesterone, and to a lesser extent, estrone to 17beta-estradiol. We established MCF-7 cells that stably express AKR1C3 (MCF-7-AKR1C3 cells) to model its over-expression in breast cancer. AKR1C3 expression increased steroid conversion by MCF-7 cells, leading to a pro-estrogenic state. Unexpectedly, estrone was reduced fastest by MCF-7-AKR1C3 cells when compared to other substrates at 0.1muM. MCF-7-AKR1C3 cells proliferated three times faster than parental cells in response to estrone and 17beta-estradiol. AKR1C3 therefore represents a potential target for attenuating estrogen receptor alpha induced proliferation. MCF-7-AKR1C3 cells also reduced PGD(2), limiting its dehydration to form PGJ(2) products. The AKR1C3 product was confirmed as 9alpha,11beta-PGF(2) and quantified with a stereospecific stable isotope dilution liquid chromatography-mass spectrometry method. This method will allow the examination of the role of AKR1C3 in endogenous prostaglandin formation in response to inflammatory stimuli. Expression of AKR1C3 reduced the anti-proliferative effects of PGD(2) on MCF-7 cells, suggesting that AKR1C3 limits peroxisome proliferator activated receptor gamma (PPARgamma) signaling by reducing formation of 15-deoxy-Delta(12,14)-PGJ(2) (15dPGJ(2)).
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.