ArticleThe Journal of experimental medicine2017
AKR1B1 promotes basal-like breast cancer progression by a positive feedback loop that activates the EMT program.
Article in The Journal of experimental medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 169 citations in OpenAlex.
- Prostaglandins regulate the nucleoskeleton during Drosophila border cell migration.bioRxiv : the preprint server for biology · 2026Article
- AKR1B1 promotes canine mammary tumorigenesis via activation of PI3K/AKT signaling and acts as a serum biomarker.Scientific reports · 2026Article
- Clinical impact of the methylation status of SMAD4 and AKR1B1 genes in a liquid biopsy sample as a prognostic marker for breast cancer.Scientific reports · 2026Article
- Lactylation of Mutation-Prone RAS Residues Mimics Oncogenic Mutations and Drives Constitutive Activation.Cancer communications (London, England) · 2026Article
- AKR1B1 is Required for Maintaining Acute Leukemia Cell Survival by Epigenetic Silencing of Tumor Suppressor Genes.Biochemical genetics · 2025Article
- RHOA lactylation at oncogenic hotspots promotes oncogenic activity and protein stabilization.Molecular cancer · 2025Article
- Aldose Reductase Involvement in EMT: Emerging Insights and Current Proposed Molecular Mechanisms.Biology · 2025Review
- Metabolomics as a tool for understanding and treating triple-negative breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- AKR1B10 as a novel prognostic biomarker linking methylation and immune escape in hepatocellular carcinoma.Discover oncology · 2025Article
- Targeting AKR1B1 inhibits metabolic reprogramming to reverse systemic therapy resistance in hepatocellular carcinoma.Signal transduction and targeted therapy · 2025Article
- ERCC1/NGFR affects prognosis in basal-like breast cancer.European journal of medical research · 2025Article
- AKR1B1 Expression in the Colorectal Tumor Microenvironment Contributes Towards Its Prognostic Significance.Cancer medicine · 2025Article
- Repurposing of epalrestat for neuroprotection in parkinson's disease via activation of the KEAP1/Nrf2 pathway.Journal of neuroinflammation · 2025Article
- The Role of Claudin-1 in Enhancing Pancreatic Cancer Aggressiveness and Drug Resistance via Metabolic Pathway Modulation.Cancers · 2025Article
- Polyol pathway-generated fructose is indispensable for growth and survival of non-small cell lung cancer.Cell death and differentiation · 2025Article
- Deciphering molecular pathways driving cancer invasion and metastasis: advances and therapeutic prospects.Frontiers in oncology · 2025Review
- Exploring fructose metabolism as a potential therapeutic approach for pancreatic cancer.Cell death and differentiation · 2024Article
- NADPHnet: a novel strategy to predict compounds for regulation of NADPH metabolism via network-based methods.Acta pharmacologica Sinica · 2024Article
- AMD1 promotes breast cancer aggressiveness via a spermidine-eIF5A hypusination-TCF4 axis.Breast cancer research : BCR · 2024Article
- The polyol pathway and nuclear ketohexokinase A signaling drive hyperglycemia-induced metastasis of gastric cancer.Experimental & molecular medicine · 2024Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Basal-like breast cancer (BLBC) is associated with high-grade, distant metastasis and poor prognosis. Elucidating the determinants of aggressiveness in BLBC may facilitate the development of novel interventions for this challenging disease. In this study, we show that aldo-keto reductase 1 member B1 (AKR1B1) overexpression highly correlates with BLBC and predicts poor prognosis in breast cancer patients. Mechanistically, Twist2 transcriptionally induces AKR1B1 expression, leading to nuclear factor κB (NF-κB) activation. In turn, NF-κB up-regulates Twist2 expression, thereby fulfilling a positive feedback loop that activates the epithelial-mesenchymal transition program and enhances cancer stem cell (CSC)-like properties in BLBC. AKR1B1 expression promotes, whereas AKR1B1 knockdown inhibits, tumorigenicity and metastasis. Importantly, epalrestat, an AKR1B1 inhibitor that has been approved for the treatment of diabetic complications, significantly suppresses CSC properties, tumorigenicity, and metastasis of BLBC cells. Together, our study identifies AKR1B1 as a key modulator of tumor aggressiveness and suggests that pharmacologic inhibition of AKR1B1 has the potential to become a valuable therapeutic strategy for BLBC.
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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.