ArticleThe Journal of clinical investigation2022
Stromal oncostatin M cytokine promotes breast cancer progression by reprogramming the tumor microenvironment.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 55 citations in OpenAlex.
- Inflammatory bowel disease and breast cancer: epidemiological evidence, shared biology, and clinical management.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Oncostatin M as a Multifunctional Regulator of Breast Cancer Progression: Current Insights and Future Therapeutic Avenues.IUBMB life · 2026Review
- Fibroblastic aspartoacylase suppresses TGFβ-mediated responses and cancer progression.Nature communications · 2026Article
- Integrating Radiomics and Computational Pathology to Predict Early Recurrence of Pancreatic Ductal Adenocarcinoma and Uncover Its Biological Basis in Tumor Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Multi-omics profiling identifies ectopic olfactory receptors as putative drivers of tumor progression and prognostic indicators in clear cell renal cell carcinoma.Clinical and experimental medicine · 2026Article
- Oncostatin-M ligand-based CAR-T therapy displays robust anti-tumor activity against osteosarcoma.BMC medicine · 2026Article
- Immunotherapy drug target identification using machine learning and patient-derived tumour explant validation.Nature machine intelligence · 2026Article
- Next Generation DNA Damage Response Inhibitors: Harnessing Nanocarriers and Tumor Microenvironment for Precision Cancer Therapy.Oncology research · 2026Review
- Oncostatin M induced by STAT5-activating oncogenes promotes disease progression in hematologic malignancies.Signal transduction and targeted therapy · 2025Article
- Sema7a drives an immunosuppressive microenvironment of breast cancer via Kdm4a-mediated DNA replication regulation.Communications biology · 2025Article
- Investigating Germ Cell Transition Genes in Breast Cancer: Exploring the Genesis of Cancer Testis-Associated Markers.International journal of molecular sciences · 2025Article
- Discovery of a Linked Constellation of Gene Expression Revealed by Local Editing of Fibroblasts in Tumors.bioRxiv : the preprint server for biology · 2025Article
- Lovastatin inhibits adipocyte-associated increased proliferation, EMT and aggressiveness of breast cancer cells.Medical oncology (Northwood, London, England) · 2025Article
- Cytokine-centered strategies to boost cancer immunotherapy.Molecular oncology · 2025Review
- Transcriptomic analysis reveals the key role of inflammatory and immune signaling in the anti-perimenopausal depression effects of Bushen Shugan Huayu decoction.Frontiers in psychiatry · 2025Article
- Multi-Omics Analysis Reveals the transforming growth factor-β Signaling-Driven Multicellular Interactions with Prognostic Relevance in Cervical Cancer Progression.Journal of Cancer · 2025Article
- Nanoparticles Modulating the Immune Microenvironment in Breast Cancer Treatment.International journal of nanomedicine · 2025Review
- Toll-Like receptor 3-mediated interferon-β production is suppressed by oncostatin m and a broader epithelial-mesenchymal transition program.Breast cancer research : BCR · 2024Article
- Advanced machine learning unveils CD8 + T cell genetic markers enhancing prognosis and immunotherapy efficacy in breast cancer.BMC cancer · 2024Article
- Performance comparison of high throughput single-cell RNA-Seq platforms in complex tissues.Heliyon · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
30 authors at 13 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor microenvironment (TME) is reprogrammed by cancer cells and participates in all stages of tumor progression. The contribution of stromal cells to the reprogramming of the TME is not well understood. Here, we provide evidence of the role of the cytokine oncostatin M (OSM) as central node for multicellular interactions between immune and nonimmune stromal cells and the epithelial cancer cell compartment. OSM receptor (OSMR) deletion in a multistage breast cancer model halted tumor progression. We ascribed causality to the stromal function of the OSM axis by demonstrating reduced tumor burden of syngeneic tumors implanted in mice lacking OSMR. Single-cell and bioinformatic analysis of murine and human breast tumors revealed that OSM expression was restricted to myeloid cells, whereas OSMR was detected predominantly in fibroblasts and, to a lower extent, cancer cells. Myeloid-derived OSM reprogrammed fibroblasts to a more contractile and tumorigenic phenotype and elicited the secretion of VEGF and proinflammatory chemokines CXCL1 and CXCL16, leading to increased myeloid cell recruitment. Collectively, our data support the notion that the stromal OSM/OSMR axis reprograms the immune and nonimmune microenvironment and plays a key role in breast cancer 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.