ArticleProceedings of the National Academy of Sciences of the United States of America2020
The functional activity of E-cadherin controls tumor cell metastasis at multiple steps.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 257 papers, 1 of them a synthesis that pooled it.
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Who cites it
257 citing papers in PubMed, 1 synthesis or guideline pooled it, 444 citations in OpenAlex.
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- Pharmacological activation of dopamine receptor D1 attenuates TGF-β-induced epithelial-mesenchymal transition in A549 and BEAS-2B cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
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- Syndesmos functions as a tumor suppressor by facilitating epithelial cell adhesion mediated by interactions of E-cadherin and β-catenin.Cell death & disease · 2026Article
- Automatic Blood Protein Enrichment by Magnetic-COF Polymers.Analytical chemistry · 2026Article
- Inflammation-Driven JNK Activation Promotes EMT and Metastasis in Gastric Cancer and Is Attenuated by Huangjin Shuangshen Granules.Pharmaceuticals (Basel, Switzerland) · 2026Article
- PSMC2 serves as a potential regulatory target of EZH2 in promoting glioma progression via epithelial-mesenchymal transition.Scientific reports · 2026Article
- Suppressive role of SCN4B in the epithelial‑mesenchymal transition of lung adenocarcinoma.Oncology reports · 2026Article
- Low E-cadherin expression is associated with poor prognosis in pulmonal adenocarcinoma.Scientific reports · 2026Article
197 more citing papers are in PubMed but not listed here.
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4 authors at 2 institutions in 1 country.
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Abstract
E-cadherin is a tumor suppressor protein, and the loss of its expression in association with the epithelial mesenchymal transition (EMT) occurs frequently during tumor metastasis. However, many metastases continue to express E-cadherin, and a full EMT is not always necessary for metastasis; also, positive roles for E-cadherin expression in metastasis have been reported. We hypothesize instead that changes in the functional activity of E-cadherin expressed on tumor cells in response to environmental factors is an important determinant of the ability of the tumor cells to metastasize. We find that E-cadherin expression persists in metastatic lung nodules and circulating tumor cells (CTCs) in two mouse models of mammary cancer: genetically modified MMTV-PyMT mice and orthotopically grafted 4T1 tumor cells. Importantly, monoclonal antibodies that bind to and activate E-cadherin at the cell surface reduce lung metastasis from endogenous genetically driven tumors and from tumor cell grafts. E-cadherin activation inhibits metastasis at multiple stages, including the accumulation of CTCs from the primary tumor and the extravasation of tumor cells from the vasculature. These activating mAbs increase cell adhesion and reduce cell invasion and migration in both cell culture and three-dimensional spheroids grown from primary tumors. Moreover, activating mAbs increased the frequency of apoptotic cells without affecting proliferation. Although the growth of the primary tumors was unaffected by activating mAbs, CTCs and tumor cells in metastatic nodules exhibited increased apoptosis. Thus, the functional state of E-cadherin is an important determinant of metastatic potential beyond whether the gene is expressed.
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