ArticleBritish journal of cancer2023
Loss of alcohol dehydrogenase 1B in cancer-associated fibroblasts: contribution to the increase of tumor-promoting IL-6 in colon cancer.
Article in British journal of cancer, 2023. 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, 10 citations in OpenAlex.
- Article
- Targeting Cancer-Associated Fibroblasts with Small-Molecule Inhibitors: Molecular Mechanisms and Therapeutic Potential.Drug design, development and therapy · 2026Review
- Development and validation of a CAF-related signature for prognosis and therapy response in colorectal cancer: new insights on HSPB1.NPJ precision oncology · 2025Article
- Identification of glycolysis-related genes and analysis of potential prognostic clinical application in oral squamous cell carcinoma.Translational cancer research · 2025Article
- The Hypoxia-Retinoid Axis in Idiopathic Pulmonary Fibrosis: Multifaceted Etiology and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Identification and Validation of the Potential Key Biomarkers for Atopic Dermatitis Mitochondrion by Learning Algorithms.Journal of inflammation research · 2025Article
- Disruption of retinol-mediated IL-6 expression in colon cancer-associated fibroblasts: new perspectives on the role of vitamin A metabolism.Oncotarget · 2023Article
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
Abstract
backgroundIncreases in IL-6 by cancer-associated fibroblasts (CAFs) contribute to colon cancer progression, but the mechanisms involved in the increase of this tumor-promoting cytokine are unknown. The aim of this study was to identify novel targets involved in the dysregulation of IL-6 expression by CAFs in colon cancer.
methodsColonic normal (N), hyperplastic, tubular adenoma, adenocarcinoma tissues, and tissue-derived myo-/fibroblasts (MFs) were used in these studies.
resultsTranscriptomic analysis demonstrated a striking decrease in alcohol dehydrogenase 1B (ADH1B) expression, a gene potentially involved in IL-6 dysregulation in CAFs. ADH1B expression was downregulated in approximately 50% of studied tubular adenomas and all T1-4 colon tumors, but not in hyperplastic polyps. ADH1B metabolizes alcohols, including retinol (RO), and is involved in the generation of all-trans retinoic acid (atRA). LPS-induced IL-6 production was inhibited by either RO or its byproduct atRA in N-MFs, but only atRA was effective in CAFs. Silencing ADH1B in N-MFs significantly upregulated LPS-induced IL-6 similar to those observed in CAFs and lead to the loss of RO inhibitory effect on inducible IL-6 expression.
conclusionOur data identify ADH1B as a novel potential mesenchymal tumor suppressor, which plays a critical role in ADH1B/retinoid-mediated regulation of tumor-promoting IL-6.
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