ReviewJournal of clinical medicine2016
Homeostatic Signaling by Cell-Cell Junctions and Its Dysregulation during Cancer Progression.
Review in Journal of clinical medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed.
- Article
- Integrated airway epithelial signaling networks linking allergen-driven inflammation to airway remodeling in asthma.Frontiers in immunology · 2026Review
- Actin-dependent recruitment of AGO2 to the zonula adherens.Molecular biology of the cell · 2023Article
- Sctensor detects many-to-many cell-cell interactions from single cell RNA-sequencing data.BMC bioinformatics · 2023Article
- The hTERT-p50 homodimer inhibits PLEKHA7 expression to promote gastric cancer invasion and metastasis.Oncogene · 2023Article
- DUSP3 regulates phosphorylation-mediated degradation of occludin and is required for maintaining epithelial tight junction.Journal of biomedical science · 2022Article
- Footprints of microRNAs in Cancer Biology.Biomedicines · 2021Review
- PIGNON: a protein-protein interaction-guided functional enrichment analysis for quantitative proteomics.BMC bioinformatics · 2021Article
- The Colonic Mucosal MicroRNAs, MicroRNA-219a-5p, and MicroRNA-338-3p Are Downregulated in Irritable Bowel Syndrome and Are Associated With Barrier Function and MAPK Signaling.Gastroenterology · 2021Article
- Using dynamic cell communication improves treatment strategies of breast cancer.Cancer cell international · 2021Review
- Prolonged Exposure to Platelet Activating Factor Transforms Breast Epithelial Cells.Frontiers in genetics · 2021Article
- PDSS2-Del2, a new variant of PDSS2, promotes tumor cell metastasis and angiogenesis in hepatocellular carcinoma via activating NF-κB.Molecular oncology · 2020Article
- SVFX: a machine learning framework to quantify the pathogenicity of structural variants.Genome biology · 2020Article
- From Orai to E-Cadherin: Subversion of Calcium Trafficking in Cancer to Drive Proliferation, Anoikis-Resistance, and Metastasis.Biomedicines · 2020Review
- Identification of Potential Therapeutic Targets and Immune Cell Infiltration Characteristics in Osteosarcoma Using Bioinformatics Strategy.Frontiers in oncology · 2020Article
- Cell-cell junctions in developing and adult tendons.Tissue barriers · 2020Article
- PTPN13 induces cell junction stabilization and inhibits mammary tumor invasiveness.Theranostics · 2020Article
- The KN Motif and Ankyrin Repeat Domains 1/CXXC Finger Protein 5 Axis Regulates Epithelial-Mesenchymal Transformation, Metastasis and Apoptosis of Gastric Cancer via Wnt Signaling.OncoTargets and therapy · 2020Article
- Schwann cells support oncogenic potential of pancreatic cancer cells through TGFβ signaling.Cell death & disease · 2019Article
- Mechanical Force Induces Phosphorylation-Mediated Signaling that Underlies Tissue Response and Robustness in Xenopus Embryos.Cell systems · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The transition of sessile epithelial cells to a migratory, mesenchymal phenotype is essential for metazoan development and tissue repair, but this program is exploited by tumor cells in order to escape the confines of the primary organ site, evade immunosurveillance, and resist chemo-radiation. In addition, epithelial-to-mesenchymal transition (EMT) confers stem-like properties that increase efficiency of colonization of distant organs. This review evaluates the role of cell-cell junctions in suppressing EMT and maintaining a quiescent epithelium. We discuss the conflicting data on junctional signaling in cancer and recent developments that resolve some of these conflicts. We focus on evidence from breast cancer, but include other organ sites where appropriate. Current and potential strategies for inhibition of EMT are discussed.
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What OpenQuestion holds
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.