ArticleCancer research2011
c-MYC functions as a molecular switch to alter the response of human mammary epithelial cells to oncostatin M.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Human platelet lysate enhances in vivo activity of CAR-Vδ2 T cells by reducing cellular senescence and apoptosis.Cytotherapy · 2024Article
- c-MYC mediates the crosstalk between breast cancer cells and tumor microenvironment.Cell communication and signaling : CCS · 2023Review
- The clinical relevance of OSM in inflammatory diseases: a comprehensive review.Frontiers in immunology · 2023Review
- Activation of OSM-STAT3 Epigenetically Regulates Tumor-Promoting Transcriptional Programs in Cervical Cancer.Cancers · 2022Article
- Stromal oncostatin M cytokine promotes breast cancer progression by reprogramming the tumor microenvironment.The Journal of clinical investigation · 2022Article
- The Role of the IL-6 Cytokine Family in Epithelial-Mesenchymal Plasticity in Cancer Progression.International journal of molecular sciences · 2021Review
- Aberrant Induction of a Mesenchymal/Stem Cell Program Engages Senescence in Normal Mammary Epithelial Cells.Molecular cancer research : MCR · 2021Article
- Emerging Perspectives on Leukemia Inhibitory Factor and its Receptor in Cancer.Frontiers in oncology · 2021Review
- OSMR controls glioma stem cell respiration and confers resistance of glioblastoma to ionizing radiation.Nature communications · 2020Article
- A FAM83A Positive Feed-back Loop Drives Survival and Tumorigenicity of Pancreatic Ductal Adenocarcinomas.Scientific reports · 2019Article
- Article
- Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling.Oncogene · 2017Article
- Potent EMT and CSC Phenotypes Are Induced By Oncostatin-M in Pancreatic Cancer.Molecular cancer research : MCR · 2017Article
- Oncostatin M activation of Stat3:Smad3 complexes drives senescence.Cell cycle (Georgetown, Tex.) · 2017Article
- STAT3-mediated SMAD3 activation underlies Oncostatin M-induced Senescence.Cell cycle (Georgetown, Tex.) · 2017Article
- Effect of human papillomavirus 16 oncoproteins on oncostatin M upregulation in oral squamous cell carcinoma.Medical oncology (Northwood, London, England) · 2016Article
- Review
- STAT3 in Cancer-Friend or Foe?Cancers · 2014Article
- Article
- Oncostatin M receptor is a novel therapeutic target in cervical squamous cell carcinoma.The Journal of pathology · 2014Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Cytokines play an important role in creating an inflammatory microenvironment, which is now considered a hallmark of cancer. Although tumor cells can exploit cytokine signaling to promote growth, invasion, and metastasis, the response of normal and premalignant epithelial cells to cytokines present in a developing tumor microenvironment remains unclear. Oncostatin M (OSM), an IL-6 family cytokine responsible for STAT3 activation, has been implicated in cancer development, progression, invasion, and metastasis. Paradoxically, OSM can also suppress the growth of normal cells and certain tumor-derived cell lines. Using isogenic human mammary epithelial cells (HMEC) at different stages of neoplastic transformation, we found that OSM signaling suppressed c-MYC expression and engaged a p16- and p53-independent growth arrest that required STAT3 activity. Inhibition of STAT3 activation by expressing a dominant-negative STAT3 protein or a STAT3-shRNA prevented the OSM-mediated arrest. In addition, expression of c-MYC from a constitutive promoter also abrogated the STAT3-mediated arrest, and strikingly, cooperated with OSM to promote anchorage-independent growth (AIG), a property associated with malignant transformation. Cooperative transformation by c-MYC and OSM required PI3K and AKT signaling, showing the importance of multiple signaling pathways downstream of the OSM receptor in defining the cellular response to cytokines. These findings identify c-MYC as an important molecular switch that alters the cellular response to OSM-mediated signaling from tumor suppressive to tumor promoting.
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Registered trials
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.