ArticleClinical & experimental metastasis2012
Hepatocyte induced re-expression of E-cadherin in breast and prostate cancer cells increases chemoresistance.
Article in Clinical & experimental metastasis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 90 citations in OpenAlex.
- Weekly low-dose docetaxel combined with estramustine and dexamethasone for Japanese patients with metastatic castration-resistant prostate cancer.International journal of clinical oncology · 2013Trial
- E-cadherin-driven adherens junction reinforcement promotes spheroid-mediated invasion and progression in ALK-rearranged lung cancer chemoresistance.Molecules and cells · 2026Article
- Unique Cohorts of Salivary Gland Cancer Cells as anJournal of maxillofacial and oral surgery · 2024Article
- Mesenchymal Stem Cell-Secreted Exosomes and Soluble Signals Regulate Breast Cancer Metastatic Dormancy: Current Progress and Future Outlook.International journal of molecular sciences · 2024Review
- Mechanisms of Organ-Specific Metastasis of Breast Cancer.Cold Spring Harbor perspectives in medicine · 2023Review
- Analysis of the metastatic mechanism and progress in the treatment of breast cancer liver metastasis: a narrative review.Translational cancer research · 2023Review
- Exogenous growth hormone promotes an epithelial-mesenchymal hybrid phenotype in cancerous HeLa cells but not in non-cancerous HEK293 cells.Molecular and cellular biochemistry · 2023Article
- Possible Mechanisms of Resistance Development to Photodynamic Therapy (PDT) In Vulvar Cancer Cells.International journal of molecular sciences · 2022Article
- Interferon-γ increases sensitivity to chemotherapy and provides immunotherapy targets in models of metastatic castration-resistant prostate cancer.Scientific reports · 2022Article
- Thorny ground, rocky soil: Tissue-specific mechanisms of tumor dormancy and relapse.Seminars in cancer biology · 2022Review
- Breast cancer liver metastasis: Pathogenesis and clinical implications.Frontiers in oncology · 2022Review
- In 2D and 3D Cell Culture Models, Effects of Endothelial Cells on E-cadherin / β-catenin Expression Levels and Spheroid Sizes in Ishikawa Cells.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Autophagy and Hepatic Tumor Microenvironment Associated Dormancy.Journal of gastrointestinal cancer · 2021Review
- Circulating Tumour Cells (CTCs) in NSCLC: From Prognosis to Therapy Design.Pharmaceutics · 2021Review
- Review
- Phenotypic Heterogeneity of Triple-Negative Breast Cancer Mediated by Epithelial-Mesenchymal Plasticity.Cancers · 2021Review
- A Perspective on Therapeutic Pan-Resistance in Metastatic Cancer.International journal of molecular sciences · 2020Review
- Expression of E-cadherin and specific CXCR3 isoforms impact each other in prostate cancer.Cell communication and signaling : CCS · 2019Article
- Controversies around epithelial-mesenchymal plasticity in cancer metastasis.Nature reviews. Cancer · 2019Review
- PRRX1 Regulates Cellular Phenotype Plasticity and Dormancy of Head and Neck Squamous Cell Carcinoma Through miR-642b-3p.Neoplasia (New York, N.Y.) · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Post-extravasation survival is a key rate-limiting step of metastasis; however, not much is known about the factors that enable survival of the metastatic cancer cell at the secondary site. Furthermore, metastatic nodules are often refractory to current therapies, necessitating the elucidation of molecular changes that affect the chemosensitivity of metastases. Drug resistance exhibited by tumor spheroids has been shown to be mediated by cell adhesion and can be abrogated by addition of E-cadherin blocking antibody. We have previously shown that hepatocyte coculture induces the re-expression of E-cadherin in breast and prostate cancer cells. In this study, we show that this E-cadherin re-expression confers a survival advantage, particularly in the liver microenvironment. E-cadherin re-expression in MDA-MB-231 breast cancer cells resulted in increased attachment to hepatocytes. This heterotypic adhesion between cancer cells and secondary organ parenchymal cells activated ERK MAP kinase, suggesting a functional pro-survival role for E-cadherin during metastatic colonization of the liver. In addition, breast cancer cells that re-expressed E-cadherin in hepatocyte coculture were more chemoresistant compared to 231-shEcad cells unable to re-express E-cadherin. Similar results were obtained in DU-145 prostate cancer cells induced to re-express E-cadherin in hepatocyte coculture or following chemical induction by the GnRH agonist buserelin or the EGFR inhibitor PD153035. These results suggest that E-cadherin re-expression and other molecular changes imparted by a partial mesenchymal to epithelial reverting transition at the secondary site increase post-extravasation survival of the metastatic cancer cell and may help to elucidate why chemotherapy commonly fails to treat metastatic breast cancer.
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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.