ArticleOncogene2017
Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.
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Who cites it
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.
- Mechanisms of obesity- and diabetes mellitus-related pancreatic carcinogenesis: a comprehensive and systematic review.Signal transduction and targeted therapy · 2023Pooled it
- Spatial analysis of head and neck cancer identifies two ecosystems with distinct modes of epithelial-to-mesenchymal transition.Nature genetics · 2026Article
- The role of cytokines in ovarian cancer drug resistance.International journal of cancer · 2026Review
- Patient-derived orthotopic xenograft models recapitulate the peritoneal dissemination of pancreatic cancer and delineate its transcriptional and regulatory programs.Journal of experimental & clinical cancer research : CR · 2026Article
- Tumor Microenvironment Onmyoji: Cytokines with Dual Protumor and Antitumor Roles.Cancer communications (London, England) · 2026Review
- Oncostatin M induced by STAT5-activating oncogenes promotes disease progression in hematologic malignancies.Signal transduction and targeted therapy · 2025Article
- Glioportal: a comprehensive transcriptomic resource unveiling ligand-mediated mesenchymal transition in glioblastoma.Neuro-oncology · 2025Article
- Cancer stem cells: landscape, challenges and emerging therapeutic innovations.Signal transduction and targeted therapy · 2025Review
- Relationships between tumor CD147 expression, tumor-infiltrating lymphocytes, and oncostatin M in hepatocellular carcinoma.Virchows Archiv : an international journal of pathology · 2025Article
- The Diverse Function of IL-6 in Biological Processes and the Advancement of Cancer.Immune network · 2025Review
- The IL-22-oncostatin M axis promotes intestinal inflammation and tumorigenesis.Nature immunology · 2025Article
- Article
- 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
- 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
- Blocking Oncostatin M receptor abrogates STAT3 mediated integrin signaling and overcomes chemoresistance in ovarian cancer.NPJ precision oncology · 2024Article
- TGF-β1 induces PD-1 expression in macrophages through SMAD3/STAT3 cooperative signaling in chronic inflammation.JCI insight · 2024Article
- Cancer cell plasticity: from cellular, molecular, and genetic mechanisms to tumor heterogeneity and drug resistance.Cancer metastasis reviews · 2024Review
- Tumor-educated Gr1+CD11b+ cells drive breast cancer metastasis via OSM/IL-6/JAK-induced cancer cell plasticity.The Journal of clinical investigation · 2024Article
- Effects of Exercise-Induced Changes in Myokine Expression on the Tumor Microenvironment.Sports medicine international open · 2024Review
- Intraoperative radiotherapy in breast cancer: Alterations to the tumor microenvironment and subsequent biological outcomes (Review).Molecular medicine reports · 2023Review
31 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Increasing evidence supports the idea that cancer cell plasticity promotes metastasis and tumor recurrence, resulting in patient mortality. While it is clear that the tumor microenvironment (TME) contributes to cancer cell plasticity, the specific TME factors most actively controlling plasticity remain largely unknown. Here, we performed a screen to identify TME cytokines and growth factors that promote epithelial-mesenchymal plasticity, and acquisition of cancer stem cell (CSC) properties. Of 28 TME cytokines and growth factors tested, we identified Oncostatin M (OSM) as the most potent inducer of mesenchymal/CSC properties. OSM-induced plasticity was Signal Transducer and Activator of Transcription 3 (STAT3)-dependent, and also required a novel intersection with transforming growth factor-β (TGF-β)/SMAD signaling. OSM/STAT3 activation promoted SMAD3 nuclear accumulation, DNA binding and induced SMAD3-dependent transcriptional activity. Suppression of TGF-β receptor activity or ablation of SMAD3 or SMAD4, but not SMAD2, strongly suppressed OSM/STAT3-mediated plasticity. Moreover, removal of OSM or inhibition of STAT3 or SMAD3 resulted in a marked reversion to a non-invasive, epithelial phenotype. We propose that targeted blockade of the STAT3/SMAD3 axis in tumor cells may represent a novel therapeutic approach to prevent the plasticity required for metastatic progression and tumor recurrence.
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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.