ArticleCancer informatics2015
Regulation of epithelial-mesenchymal transition in breast cancer cells by cell contact and adhesion.
Article in Cancer informatics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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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Who cites it
35 citing papers in PubMed, 55 citations in OpenAlex.
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- Epithelial Cell Mechanoresponse to Matrix Viscoelasticity and Confinement Within Micropatterned Viscoelastic Hydrogels.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A Boolean network model of hypoxia, mechanosensing and TGF-β signaling captures the role of phenotypic plasticity and mutations in tumor metastasis.PLoS computational biology · 2025Article
- Review
- Emerging functions of C/EBPβ in breast cancer.Frontiers in oncology · 2023Review
- Discovery of a tetrahydroisoquinoline-based CDK9-cyclin T1 protein-protein interaction inhibitor as an anti-proliferative and anti-migration agent against triple-negative breast cancer cells.Genes & diseases · 2022Article
- Review
- Integrin-linked kinase tunes cell-cell and cell-matrix adhesions to regulate the switch between apoptosis and EMT downstream of TGFβ1.Molecular biology of the cell · 2021Article
- Impact of Nischarin on EMT regulators in breast cancer cell lines.Oncology letters · 2020Article
- Identification of miR-515-3p and its targets, vimentin and MMP3, as a key regulatory mechanism in esophageal cancer metastasis: functional and clinical significance.Signal transduction and targeted therapy · 2020Article
- Article
- Transcriptome of Two Canine Prostate Cancer Cells Treated With Toceranib Phosphate Reveals Distinct Antitumor Profiles Associated With the PDGFR Pathway.Frontiers in veterinary science · 2020Article
- P120 Catenin Isoforms Differentially Associate with Breast Cancer Invasion and Metastasis.Cancers · 2019Article
- Cooperativity between stromal cytokines drives the invasive migration of human breast cancer cells.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Article
- Article
- PRSS3/Mesotrypsin and kallikrein-related peptidase 5 are associated with poor prognosis and contribute to tumor cell invasion and growth in lung adenocarcinoma.Scientific reports · 2019Article
- RAC1B: A Rho GTPase with Versatile Functions in Malignant Transformation and Tumor Progression.Cells · 2019Review
- Defining rules for cancer cell proliferation in TRAIL stimulation.NPJ systems biology and applications · 2019Article
- A High-Content Screening Approach to Identify MicroRNAs Against Head and Neck Cancer Cell Survival and EMT in an Inflammatory Microenvironment.Frontiers in oncology · 2019Article
- Blockade of ARHGAP11A reverses malignant progress via inactivating Rac1B in hepatocellular carcinoma.Cell communication and signaling : CCS · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) is a physiological program that is activated during cancer cell invasion and metastasis. We show here that EMT-related processes are linked to a broad and conserved program of transcriptional alterations that are influenced by cell contact and adhesion. Using cultured human breast cancer and mouse mammary epithelial cells, we find that reduced cell density, conditions under which cell contact is reduced, leads to reduced expression of genes associated with mammary epithelial cell differentiation and increased expression of genes associated with breast cancer. We further find that treatment of cells with matrix metalloproteinase-3 (MMP-3), an inducer of EMT, interrupts a defined subset of cell contact-regulated genes, including genes encoding a variety of RNA splicing proteins known to regulate the expression of Rac1b, an activated splice isoform of Rac1 known to be a key mediator of MMP-3-induced EMT in breast, lung, and pancreas. These results provide new insights into how MMPs act in cancer progression and how loss of cell-cell interactions is a key step in the earliest stages of cancer development.
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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.