ArticleOncotarget2016
A high-content EMT screen identifies multiple receptor tyrosine kinase inhibitors with activity on TGFβ receptor.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Transforming growth factor-β and integrins: key players in EMT and breast cancer progression.Cancer cell international · 2026Review
- A morphology-based machine learning model for scoring epithelial-mesenchymal plasticity using organelle dynamics.Communications biology · 2025Article
- Investigating the Role of TGF-β Signaling Pathways in Human Corneal Endothelial Cell Primary Culture.Cells · 2023Article
- Pooled genetic screens with image-based profiling.Molecular systems biology · 2022Review
- Review
- A dual role of Irf1 in maintaining epithelial identity but also enabling EMT and metastasis formation of breast cancer cells.Oncogene · 2020Article
- Caveolae, CD109, and endothelial cells as targets for treating Alzheimer's disease.Alzheimer's & dementia (New York, N. Y.) · 2020Article
- Primary cell-based phenotypic assays to pharmacologically and genetically study fibrotic diseasesJournal of biological methods · 2019Article
- A kinome-wide high-content siRNA screen identifies MEK5-ERK5 signaling as critical for breast cancer cell EMT and metastasis.Oncogene · 2018Article
- miR-1199-5p and Zeb1 function in a double-negative feedback loop potentially coordinating EMT and tumour metastasis.Nature communications · 2017Article
- Angiotensin-(1-7) counteracts the transforming effects triggered by angiotensin II in breast cancer cells.Oncotarget · 2017Article
- Transcriptomic profiling and quantitative high-throughput (qHTS) drug screening of CDH1 deficient hereditary diffuse gastric cancer (HDGC) cells identify treatment leads for familial gastric cancer.Journal of translational medicine · 2017Article
- Gambogic acid suppresses cancer invasion and migration by inhibiting TGFβ1-induced epithelial-to-mesenchymal transition.Oncotarget · 2017Article
- Tetrandrine, an Activator of Autophagy, Induces Autophagic Cell Death via PKC-α Inhibition and mTOR-Dependent Mechanisms.Frontiers in pharmacology · 2017Article
- Chemical regulators of epithelial plasticity reveal a nuclear receptor pathway controlling myofibroblast differentiation.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An epithelial to mesenchymal transition (EMT) enables epithelial tumor cells to break out of the primary tumor mass and to metastasize. Understanding the molecular mechanisms driving EMT in more detail will provide important tools to interfere with the metastatic process. To identify pharmacological modulators and druggable targets of EMT, we have established a novel multi-parameter, high-content, microscopy-based assay and screened chemical compounds with activities against known targets. Out of 3423 compounds, we have identified 19 drugs that block transforming growth factor beta (TGFβ)-induced EMT in normal murine mammary gland epithelial cells (NMuMG). The active compounds include inhibitors against TGFβ receptors (TGFBR), Rho-associated protein kinases (ROCK), myosin II, SRC kinase and uridine analogues. Among the EMT-repressing compounds, we identified a group of inhibitors targeting multiple receptor tyrosine kinases, and biochemical profiling of these multi-kinase inhibitors reveals TGFBR as a thus far unknown target of their inhibitory spectrum. These findings demonstrate the feasibility of a multi-parameter, high-content microscopy screen to identify modulators and druggable targets of EMT. Moreover, the newly discovered "off-target" effects of several receptor tyrosine kinase inhibitors have important consequences for in vitro and in vivo studies and might beneficially contribute to the therapeutic effects observed in vivo.
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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.