ArticleEBioMedicine2020
Kynurenine 3-monooxygenase upregulates pluripotent genes through β-catenin and promotes triple-negative breast cancer progression.
Article in EBioMedicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 41 citations in OpenAlex.
- KS79356, a novel kynureninase inhibitor, suppresses triple-negative breast cancer progression by attenuating the TNF-α/NFκB-CD44-Akt signaling axis.Medical oncology (Northwood, London, England) · 2026Article
- MEK inhibitor cobimetinib increases calreticulin and induces immune modulation in TNBC.Journal of molecular medicine (Berlin, Germany) · 2026Article
- <p>KMO downregulation promotes hepatocellular carcinoma growth via 3‑HAA‑mediated mitochondrial mass and function imbalances</p>.International journal of oncology · 2026Article
- Role of Tryptophan Metabolism in Cancer.Cancer innovation · 2025Review
- Targeting SET to counteract Lyn activation demonstrates anti-cancer potential in diffuse large B-cell lymphoma.Clinical and experimental medicine · 2025Article
- Article
- Promising Gastric Cancer Biomarkers-Focus on Tryptophan Metabolism via the Kynurenine Pathway.International journal of molecular sciences · 2025Review
- The Adaptation of MCF-7 Breast Cancer Spheroids to the Chemotherapeutic Doxorubicin: The Dynamic Role of Phase I Drug Metabolizing Enzymes.Metabolites · 2025Article
- Review
- Breast cancer metastasis progression is associated with elevated activity of kynurenine monooxygenase and kynureninase.British journal of cancer · 2024Article
- Molecular mechanisms and therapeutic significance of Tryptophan Metabolism and signaling in cancer.Molecular cancer · 2024Review
- A Review of the Evidence for Tryptophan and the Kynurenine Pathway as a Regulator of Stem Cell Niches in Health and Disease.International journal of tryptophan research : IJTR · 2024Review
- Mitochondrial-related genes as prognostic and metastatic markers in breast cancer: insights from comprehensive analysis and clinical models.Frontiers in immunology · 2024Article
- Suppression of Ah Receptor (AhR) increases the aggressiveness of TNBC cells and 11-Cl-BBQ-activated AhR inhibits their growth.Biochemical pharmacology · 2023Article
- Involvement of the kynurenine pathway in breast cancer: updates on clinical research and trials.British journal of cancer · 2023Review
- The Interplay between Microbiota and Chemotherapy-Derived Metabolites in Breast Cancer.Metabolites · 2023Review
- Article
- The kynurenine pathway presents multi-faceted metabolic vulnerabilities in cancer.Frontiers in oncology · 2023Review
- Tryptophan and its metabolites in normal physiology and cancer etiology.The FEBS journal · 2023Review
- Tryptophan metabolism and disposition in cancer biology and immunotherapy.Bioscience reports · 2022Article
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTriple-negative breast cancer (TNBC) is aggressive and has a poor prognosis. Kynurenine 3-monooxygenase (KMO), a crucial kynurenine metabolic enzyme, is involved in inflammation, immune response and tumorigenesis. We aimed to study the role of KMO in TNBC.
methodsKMO alteration and expression data from public databases were analyzed. KMO expression levels in TNBC samples were analyzed using immunohistochemistry. Knockdown of KMO in TNBC cells was achieved by RNAi and CRISPR/Cas9. KMO functions were examined by MTT, colony-forming, transwell migration/invasion, and mammosphere assays. The molecular events were analyzed by cDNA microarrays, Western blot, quantitative real-time PCR and luciferase reporter assays. Tumor growth and metastasis were detected by orthotopic xenograft and tail vein metastasis mouse models, respectively.
findingsKMO was amplified and associated with worse survival in breast cancer patients. KMO expression levels were higher in TNBC tumors compared to adjacent normal mammary tissues. In vitro ectopic KMO expression increased cell growth, colony and mammosphere formation, migration, invasion as well as mesenchymal marker expression levels in TNBC cells. In addition, KMO increased pluripotent gene expression levels and promoter activities in vitro. Mechanistically, KMO was associated with β-catenin and prevented β-catenin degradation, thereby enhancing the transcription of pluripotent genes. KMO knockdown suppressed tumor growth and the expression levels of β-catenin, CD44 and Nanog. Furthermore, mutant KMO (known with suppressed enzymatic activity) could still promote TNBC cell migration/invasion. Importantly, mice bearing CRISPR KMO-knockdown TNBC tumors showed decreased lung metastasis and prolonged survival.
interpretationKMO regulates pluripotent genes via β-catenin and plays an oncogenic role in TNBC progression.
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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.