ArticleNeoplasia (New York, N.Y.)2013
Tumor microenvironmental signaling elicits epithelial-mesenchymal plasticity through cooperation with transforming genetic events.
Article in Neoplasia (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
The trial behind it
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
26 citing papers in PubMed, 33 citations in OpenAlex.
- Hallmarks of epithelial-mesenchymal plasticity in cancer.Molecular cancer · 2026Review
- A hybrid epithelial-mesenchymal transition program enables basal epithelial cells to bypass stress-induced stasis and contributes to a metaplastic breast cancer progenitor state.Breast cancer research : BCR · 2024Article
- Oncostatin-M and OSM-Receptor Feed-Forward Activation of MAPK Induces Separable Stem-like and Mesenchymal Programs.Molecular cancer research : MCR · 2023Article
- Review
- Metabolic Reprogramming of Colorectal Cancer Cells and the Microenvironment: Implication for Therapy.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
- Article
- ZGRF1 Is Associated with Poor Prognosis in Triple-Negative Breast Cancer and Promotes Cancer Stemness Based on Bioinformatics.OncoTargets and therapy · 2020Article
- The opposing effects of interferon-beta and oncostatin-M as regulators of cancer stem cell plasticity in triple-negative breast cancer.Breast cancer research : BCR · 2019Article
- Small-Molecule Ferroptotic Agents with Potential to Selectively Target Cancer Stem Cells.Scientific reports · 2019Article
- Downregulation of miR-205 contributes to epithelial-mesenchymal transition and invasion in triple-negative breast cancer by targeting HMGB1-RAGE signaling pathway.Anti-cancer drugs · 2019Article
- Cellular plasticity and metastasis in breast cancer: a pre- and post-malignant problem.Journal of cancer metastasis and treatment · 2019Article
- Using interferon-beta to combat cancer stem cell properties in triple negative breast cancer.Oncoscience · 2018Article
- Review
- Oncogenic Metabolism Acts as a Prerequisite Step for Induction of Cancer Metastasis and Cancer Stem Cell Phenotype.Oxidative medicine and cellular longevity · 2018Review
- Interferon-beta represses cancer stem cell properties in triple-negative breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Breast cancer complexity: implications of intratumoral heterogeneity in clinical management.Cancer metastasis reviews · 2017Review
- The reverse Warburg effect is likely to be an Achilles' heel of cancer that can be exploited for cancer therapy.Oncotarget · 2017Review
- Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling.Oncogene · 2017Article
- Evolutionary scalpels for dissecting tumor ecosystems.Biochimica et biophysica acta. Reviews on cancer · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Epithelial-to-mesenchymal transition (EMT) facilitates the escape of epithelial cancer cells from the primary tumor site, which is a key event early in metastasis. Here, we explore how extrinsic, tumor microenvironmental cytokines cooperate with intrinsic, genetic changes to promote EMT in human mammary epithelial cells (HMECs). Viral transduction of transforming genetic events into HMECs routinely generated two distinct cell populations. One population retained epithelial characteristics, while an emergent population spontaneously acquired a mesenchymal morphology and properties associated with cancer stem cells (CSCs). Interestingly, the spontaneous mesenchymal/CSCs were unable to differentiate and lacked epithelial-mesenchymal plasticity. In contrast, exposure of the transformed HMECs retaining epithelial characteristics to exogenous transforming growth factor-β (TGF-β) generated a mesenchymal/CSC population with remarkable plasticity. The TGF-β-induced mesenchymal/CSC population was dependent on the continued presence of TGF-β. Removal of TGF-β or pharmacologic or genetic inhibition of TGF-β/SMAD signaling led to the reversion of mesenchymal/CSC to epithelial/non-CSC. Our results demonstrate that targeting exogenous cytokine signaling disrupts epithelial-mesenchymal plasticity and may be an effective strategy to inhibit the emergence of circulating tumor cells. The model of epithelial-mesenchymal plasticity we describe here can be used to identify novel tumor microenvironmental factors and downstream signaling that cooperate with intrinsic genetic changes to drive metastasis. Understanding the interaction between extrinsic and intrinsic factors that regulate epithelial-mesenchymal plasticity will allow the development of new therapies that target tumor microenvironmental signals to reduce metastasis.
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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.