ArticleThe Journal of cell biology2004
Autocrine CSF-1R activation promotes Src-dependent disruption of mammary epithelial architecture.
Article in The Journal of cell biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01791387 (Dovitinib In 1st-Line Renal Cell Carcinoma, an Investigation Into Tumour GENe Status and Correlation With Efficacy - 1st Exploratory Study), which is not on this map. Cited by 57 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.
Dovitinib In 1st-Line Renal Cell Carcinoma, an Investigation Into Tumour GENe Status and Correlation With Efficacy - 1st Exploratory Study
Who cites it
57 citing papers in PubMed, 108 citations in OpenAlex.
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- CSF-1R in Cancer: More than a Myeloid Cell Receptor.Cancers · 2024Review
- A DNA-PK phosphorylation site on MET regulates its signaling interface with the DNA damage response.Oncogene · 2023Article
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- Triggering Receptor Expressed on Myeloid Cells-2 (TREM2) Interacts With Colony-Stimulating Factor 1 Receptor (CSF1R) but Is Not Necessary for CSF1/CSF1R-Mediated Microglial Survival.Frontiers in immunology · 2021Article
- High-grade mesenchymal pancreatic ductal adenocarcinoma drives stromal deactivation through CSF-1.EMBO reports · 2020Article
- ProtRank: bypassing the imputation of missing values in differential expression analysis of proteomic data.BMC bioinformatics · 2019Article
- Src activation decouples cell division orientation from cell geometry in mammalian cells.Biomaterials · 2018Article
- AZ304, a novel dual BRAF inhibitor, exerts anti-tumour effects in colorectal cancer independently of BRAF genetic status.British journal of cancer · 2018Article
- Multiplexed Exchange-PAINT imaging reveals ligand-dependent EGFR and Met interactions in the plasma membrane.Scientific reports · 2017Article
- Inhibition of the colony-stimulating-factor-1 receptor affects the resistance of lung cancer cells to cisplatin.Oncotarget · 2016Article
- Identifying three-dimensional structures of autophosphorylation complexes in crystals of protein kinases.Science signaling · 2015Article
- Autocrine CSF1R signaling mediates switching between invasion and proliferation downstream of TGFβ in claudin-low breast tumor cells.Oncogene · 2015Article
- Autocrine CSF-1R signaling drives mesothelioma chemoresistance via AKT activation.Cell death & disease · 2014Article
- The need for complex 3D culture models to unravel novel pathways and identify accurate biomarkers in breast cancer.Advanced drug delivery reviews · 2014Review
- Autocrine inhibition of the c-fms proto-oncogene reduces breast cancer bone metastasis assessed with in vivo dual-modality imaging.Experimental biology and medicine (Maywood, N.J.) · 2014Article
- Cullin 5 destabilizes Cas to inhibit Src-dependent cell transformation.Journal of cell science · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elevated coexpression of colony-stimulating factor receptor (CSF-1R) and its ligand, CSF-1, correlates with invasiveness and poor prognosis of a variety of epithelial tumors (Kacinski, B.M. 1995. Ann. Med. 27:79-85). Apart from recruitment of macrophages to the tumor site, the mechanisms by which CSF-1 may potentiate invasion are poorly understood. We show that autocrine CSF-1R activation induces hyperproliferation and a profound, progressive disruption of junctional integrity in acinar structures formed by human mammary epithelial cells in three-dimensional culture. Acini coexpressing receptor and ligand exhibit a dramatic relocalization of E-cadherin from the plasma membrane to punctate intracellular vesicles, accompanied by its loss from the Triton-insoluble fraction. Interfering with Src kinase activity, either by pharmacological inhibition or mutation of the Y561 docking site on CSF-1R, prevents E-cadherin translocation, suggesting that CSF-1R disrupts cell adhesion by uncoupling adherens junction complexes from the cytoskeleton and promoting cadherin internalization through a Src-dependent mechanism. These findings provide a mechanistic basis whereby CSF-1R could contribute to invasive progression in epithelial cancers.
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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.