ArticleTissue barriers2014
Loss of E-cadherin and epithelial to mesenchymal transition is not required for cell motility in tissues or for metastasis.
Article in Tissue barriers, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 42 citations in OpenAlex.
- IQGAP Family Proteins in Colorectal Cancer: Molecular Mechanisms and Prognostic Implications.Diagnostics (Basel, Switzerland) · 2026Review
- The diagnostic value of prostate health index combined with soluble e-cadherin for prostate cancer.Frontiers in endocrinology · 2025Article
- Exploring the role of Fusobacterium nucleatum in colorectal cancer: implications for tumor proliferation and chemoresistance.Cell communication and signaling : CCS · 2024Review
- Unique Cohorts of Salivary Gland Cancer Cells as anJournal of maxillofacial and oral surgery · 2024Article
- Activation of Chaperone-Mediated Autophagy Inhibits the Aryl Hydrocarbon Receptor Function by Degrading This Receptor in Human Lung Epithelial Carcinoma A549 Cells.International journal of molecular sciences · 2023Article
- Article
- Evaluation of Epithelial-Mesenchymal Transition Markers in Autoimmune Thyroid Diseases.International journal of molecular sciences · 2023Article
- Epithelial to Mesenchymal Transition as Mechanism of Progression of Pancreatic Cancer: From Mice to Men.Cancers · 2022Review
- Differential Impact of Membrane-Bound and Soluble Forms of the Prognostic Marker Syndecan-1 on the Invasiveness, Migration, Apoptosis, and Proliferation of Cervical Cancer Cells.Frontiers in oncology · 2022Article
- Lidocaine enhances the efficacy of palbociclib in triple-negative breast cancer.American journal of cancer research · 2022Article
- Computational model of E-cadherin clustering under force.Biophysical journal · 2021Article
- Overview of Evidence-Based Chemotherapy for Oral Cancer: Focus on Drug Resistance Related to the Epithelial-Mesenchymal Transition.Biomolecules · 2021Review
- Expression of E-Cadherin in Epithelial Cancer Cells Increases Cell Motility and Directionality through the Localization of ZO-1 during Collective Cell Migration.Bioengineering (Basel, Switzerland) · 2021Article
- Stabilized epithelial phenotype of cancer cells in primary tumors leads to increased colonization of liver metastasis in pancreatic cancer.Cell reports · 2021Article
- Potential Effect ofBiomolecules · 2021Article
- MicroRNA-941 regulates the proliferation of breast cancer cells by altering histone H3 Ser 10 phosphorylation.Scientific reports · 2020Article
- Isocorydine decrease gemcitabine-resistance by inhibiting epithelial-mesenchymal transition via STAT3 in pancreatic cancer cells.American journal of translational research · 2020Article
- A novel mechanism of plasminogen activation in epithelial and mesenchymal cells.Scientific reports · 2018Article
- EMT Subtype Influences Epithelial Plasticity and Mode of Cell Migration.Developmental cell · 2018Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Loss of E-cadherin has been long considered to be a major hallmark of epithelial-mesenchymal transition (EMT) and has been reported in various cancers. P120 catenin regulates E-cadherin stability on the cell surface and also plays a role in intracellular signaling by modulating nuclear transcription. We recently characterized the nature of interactions between p120 catenin and Mucin 1 (MUC1) in pancreatic cancer. Expression of different p120 catenin isoforms with and without MUC1 induced distinct morphologies, cell adhesion, and dynamic properties of motility along with different metastatic properties in vivo. Re-expression of p120 catenin isoform 3A in the context of MUC1 expression in a p120 catenin-deficient cell line stabilized expression of E-cadherin. However, orthotopic implantation of tumors using this stable cell line produced large metastatic lesions to the liver, which exceeded the volume of the primary tumor, suggesting down regulation of E-cadherin is not required for tumor metastasis. Here we extend those studies by showing that ectopic expression of E-cadherin does not block in vitro invasion of the pancreatic cancer cells, and instead accelerated the rate of tumor invasion. Furthermore, results from 23 cases of human pancreatic primary tumor specimens revealed that most tumors exhibiting metastatic activity retained epithelial morphology and E-cadherin gene expression. Our results indicate that loss of E-cadherin and EMT are not required for metastasis and that an epithelial morphology can be maintained during the process of tumor cell movement.
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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.