ArticleMolecular biology of the cell2009
A link between FXYD3 (Mat-8)-mediated Na,K-ATPase regulation and differentiation of Caco-2 intestinal epithelial cells.
Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 46 citations in OpenAlex.
- Repurposing Metformin for periodontal disease management as a form of oral-systemic preventive medicine.Journal of translational medicine · 2023Trial
- The functions of FXYD family members in human health and disease.Genes & diseases · 2026Review
- Multi-modal quantification of pathway activity with MAYA.Nature communications · 2023Article
- Article
- Displacement of Native FXYD Protein From NaFrontiers in oncology · 2022Article
- NaMolecules (Basel, Switzerland) · 2021Review
- Prognostic significance of sodium-potassium ATPase regulator, FXYD3, in human hepatocellular carcinoma.Oncology letters · 2018Article
- FXYD8, a Novel Regulator of Renal NaFrontiers in physiology · 2017Article
- Immune oppression array elucidating immune escape and survival mechanisms in uveal melanoma.International journal of ophthalmology · 2016Article
- Gluco-incretins regulate beta-cell glucose competence by epigenetic silencing of Fxyd3 expression.PloS one · 2014Article
- Overexpression of FXYD-3 is involved in the tumorigenesis and development of esophageal squamous cell carcinoma.Disease markers · 2013Article
- Translocation of Pseudomonas aeruginosa from the intestinal tract is mediated by the binding of ExoS to an Na,K-ATPase regulator, FXYD3.Infection and immunity · 2010Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FXYD3 (Mat-8) proteins are regulators of Na,K-ATPase. In normal tissue, FXYD3 is mainly expressed in stomach and colon, but it is also overexpressed in cancer cells, suggesting a role in tumorogenesis. We show that FXYD3 silencing has no effect on cell proliferation but promotes cell apoptosis and prevents cell differentiation of human colon adenocarcinoma cells (Caco-2), which is reflected by a reduction in alkaline phosphatase and villin expression, a change in several other differentiation markers, and a decrease in transepithelial resistance. Inhibition of cell differentiation in FXYD3-deficient cells is accompanied by an increase in the apparent Na+ and K+ affinities of Na,K-ATPase, reflecting the absence of Na,K-pump regulation by FXYD3. In addition, we observe a decrease in the maximal Na,K-ATPase activity due to a decrease in its turnover number, which correlates with a change in Na,K-ATPase isozyme expression that is characteristic of cancer cells. Overall, our results suggest an important role of FXYD3 in cell differentiation of Caco-2 cells. One possibility is that FXYD3 silencing prevents proper regulation of Na,K-ATPase, which leads to perturbation of cellular Na+ and K+ homeostasis and changes in the expression of Na,K-ATPase isozymes, whose functional properties are incompatible with Caco-2 cell differentiation.
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