ArticleThe Journal of membrane biology2014
Ouabain-induced alterations of the apical junctional complex involve α1 and β1 Na,K-ATPase downregulation and ERK1/2 activation independent of caveolae in colorectal cancer cells.
Article in The Journal of membrane biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- pNaktide reverses metabolic reprogramming and disease progression of ATP1A1-deficiency clear cell renal cell carcinoma.Cancer gene therapy · 2025Article
- Na,K-ATPase mediated and cardiotonic induced signaling in health and disease.Frontiers in physiology · 2025Review
- Ouabain - a double-edged sword in tumor development and progression? a review of half a century.Frontiers in physiology · 2025Review
- Molecular Basis of Na, K-ATPase Regulation of Diseases: Hormone and FXYD2 Interactions.International journal of molecular sciences · 2024Review
- In Vitro Study of the Multimodal Effect of NaBiomedicines · 2023Article
- A Low Dose of Ouabain Alters the Metabolic Profile of Adult Rats Experiencing Intrauterine Growth Restriction in a Sex-Specific Manner.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- Implications of Synthetic Modifications of the Cardiotonic Steroid Lactone Ring on Cytotoxicity.The Journal of membrane biology · 2021Article
- Evaluation of Cardiotonic Steroid Modulation of Cellular Cholesterol and Phospholipid.The Journal of membrane biology · 2021Article
- Cardiac Glycosides as Autophagy Modulators.Cells · 2021Review
- Preeclampsia: Cardiotonic Steroids, Fibrosis, Fli1 and Hint to Carcinogenesis.International journal of molecular sciences · 2021Review
- Anticancer and Antiviral Properties of Cardiac Glycosides: A Review to Explore the Mechanism of Actions.Molecules (Basel, Switzerland) · 2020Review
- Ouabain promotes partial epithelial to mesenchymal transition (EMT) changes in human autosomal dominant polycystic kidney disease (ADPKD) cells.Experimental cell research · 2017Article
- On the Many Actions of Ouabain: Pro-Cystogenic Effects in Autosomal Dominant Polycystic Kidney Disease.Molecules (Basel, Switzerland) · 2017Review
- Na/K Pump and Beyond: Na/K-ATPase as a Modulator of Apoptosis and Autophagy.Molecules (Basel, Switzerland) · 2017Review
- Ion dependence of Na-K-ATPase-mediated epithelial cell adhesion and migration.American journal of physiology. Cell physiology · 2015Article
- Alterations of the apical junctional complex and actin cytoskeleton and their role in colorectal cancer progression.Tissue barriersReview
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
Abstract
Studies have reported that Na,K-ATPase interacts with E-cadherin to stabilize (AJs) and regulate the expression of claudins, the main proteins present in the tight junction (TJ) in epithelial cells containing caveolae. However, the role of this ATPase in the regulation of the AJ and TJ proteins in colorectal cancer cells as well as the molecular events underlying this event in a caveolae-independent system remain undefined. In the present study, we used ouabain, a classic drug known to inhibit Na,K-ATPase, and Caco-2 cells, which are a well-established human colorectal cancer model that does not exhibit caveolae. We demonstrated that ouabain treatment resulted in a reduction of the β1 Na,K-ATPase protein and cell redistribution of the AJ proteins E-cadherin and β-catenin, as well as the α1 Na,K-ATPase subunit. Furthermore, ouabain increased claudin-3 protein levels, impaired the TJ barrier function and increased cell viability and proliferation during the early stages of treatment. Additionally, the observed ouabain-induced events were dependent on the activation of ERK1/2 signaling; but in contrast to previous studies, this signaling cascade was caveolae-independent. In conclusion, our findings strongly suggest that α1 and β1 Na,K-ATPase downregulation and ERK1/2 activation induced by ouabain are interlinked events that play an important role during cell-cell adhesion loss, which is an important step during the tumor progression of colorectal carcinomas.
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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.