ArticleThe Journal of pathology2022
Oncostatin M is overexpressed in NASH-related hepatocellular carcinoma and promotes cancer cell invasiveness and angiogenesis.
Article in The Journal of pathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- The Role of the OSM/OSMRβ Axis in Chronic Liver Disease Progression and Hepatocellular Carcinoma Development: A Focus on MASLD/MASH.International journal of molecular sciences · 2026Review
- When the Liver Flares: Inflammatory and Immunometabolic Mechanisms Driving the Transition from MASLD to MASH.Inflammation · 2026Review
- Developing a Clinically Practical Biomaterial Platform for Endogenous Liver Regeneration.Gels (Basel, Switzerland) · 2026Review
- Review
- A bibliometric analysis of trends and hotspots in Oncostatin M.Discover oncology · 2026Article
- RNA-Sequencing Reveals Two Subgroups of Eccrine Porocarcinomas and Poromas.Journal of cellular and molecular medicine · 2026Article
- Natural Products Targeting Angiogenesis and Tumor Microenvironment in Gastrointestinal Malignancies.Cells · 2026Review
- Stigmasterol Decreases Oncostatin M Production Through Suppressing PI3K/Akt/NF-κB Signaling Processes in Neutrophil-like Differentiated HL-60 Cells.Biomedicines · 2026Article
- The role of exercise-induced myokines in cancer-associated inflammation and immune regulation: mechanisms and prospects.Frontiers in sports and active living · 2026Review
- Osteopontin: a central hub in the pathogenesis and therapeutic intervention of liver disease.Annals of medicine · 2025Review
- Balancing the Cellular Inflammatory-Homeostatic Axis Through Natural Ingredient Supplementation.Nutrients · 2025Article
- Relationships between tumor CD147 expression, tumor-infiltrating lymphocytes, and oncostatin M in hepatocellular carcinoma.Virchows Archiv : an international journal of pathology · 2025Article
- Naringenin, a Food Bioactive Compound, Reduces Oncostatin M Through Blockade of PI3K/Akt/NF-κB Signal Pathway in Neutrophil-like Differentiated HL-60 Cells.Foods (Basel, Switzerland) · 2025Article
- Differential analysis of splenic immune indicators, transcriptomic profiles, and metabolomic features in pigs under liquid-solid feeding conditions.Frontiers in veterinary science · 2025Article
- From MASLD to HCC: What's in the middle?Heliyon · 2024Review
- Blocking Oncostatin M receptor abrogates STAT3 mediated integrin signaling and overcomes chemoresistance in ovarian cancer.NPJ precision oncology · 2024Article
- Article
- Canine interleukin-31 binds directly to OSMRβ with higher binding affinity than to IL-31RA.3 Biotech · 2023Article
- Macrophage-derived Osteopontin (SPP1) Protects From Nonalcoholic Steatohepatitis.Gastroenterology · 2023Article
- Metabolic Reprogramming of HCC: A New Microenvironment for Immune Responses.International journal of molecular sciences · 2023Review
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Authors and funding
21 authors at 9 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncostatin M (OSM) is a pleiotropic cytokine of the interleukin (IL)-6 family that contributes to the progression of chronic liver disease. Here we investigated the role of OSM in the development and progression of hepatocellular carcinoma (HCC) in non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH). The role of OSM was investigated in (1) selected cohorts of NAFLD/NASH HCC patients, (2) liver cancer cells exposed to human recombinant OSM or stably transfected to overexpress human OSM, (3) murine HCC xenografts, and (4) a murine NASH-related model of hepatic carcinogenesis. OSM was found to be selectively overexpressed in HCC cells of NAFLD/NASH patients, depending on tumor grade. OSM serum levels, barely detectable in patients with simple steatosis or NASH, were increased in patients with cirrhosis and more evident in those carrying HCC. In this latter group, OSM serum levels were significantly higher in the subjects with intermediate/advanced HCCs and correlated with poor survival. Cell culture experiments indicated that OSM upregulation in hepatic cancer cells contributes to HCC progression by inducing epithelial-to-mesenchymal transition and increased invasiveness of cancer cells as well as by inducing angiogenesis, which is of critical relevance. In murine xenografts, OSM overexpression was associated with slower tumor growth but an increased rate of lung metastases. Overexpression of OSM and its positive correlation with the angiogenic switch were also confirmed in a murine model of NAFLD/NASH-related hepatocarcinogenesis. Consistent with this, analysis of liver specimens from human NASH-related HCCs with vascular invasion showed that OSM was expressed by liver cancer cells invading hepatic vessels. In conclusion, OSM upregulation appears to be a specific feature of HCC arising on a NAFLD/NASH background, and it correlates with clinical parameters and disease outcome. Our data highlight a novel pro-carcinogenic contribution for OSM in NAFLD/NASH, suggesting a role of this factor as a prognostic marker and a putative potential target for therapy. © 2022 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.
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