ArticleMolecular cancer therapeutics2010
Na,K-ATPase subunits as markers for epithelial-mesenchymal transition in cancer and fibrosis.
Article in Molecular cancer therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 94 citations in OpenAlex.
- The role of Na,K‑ATPase in lung diseases (Review).Molecular medicine reports · 2025Review
- Integrative Spatial Omics for Systems-Level Mapping of Pathological Niches.bioRxiv : the preprint server for biology · 2025Article
- Identification of shared pathogenetic mechanisms between endometriosis and RSA based on comprehensive bioinformatics analysis.Journal of assisted reproduction and genetics · 2025Article
- FXYD1 was identified as a hub gene in recurrent miscarriage and involved in decidualization via regulating Na/K-ATPase activity.Journal of assisted reproduction and genetics · 2025Article
- ATP1B3 may promote glioma proliferation and migration through MAPK/NF-KB signaling pathway.Frontiers in oncology · 2025Article
- FXYD3 Is Frequently Expressed in Pancreatic Ductal Adenocarcinoma but Does Not Predict Survival.Cancer medicine · 2025Article
- An anoikis-related gene signature predicts prognosis, drug sensitivity, and immune microenvironment in cholangiocarcinoma.Heliyon · 2024Article
- Non-Professional Phagocytosis Increases in Melanoma Cells and Tissues with Increasing E-Cadherin Expression.Current oncology (Toronto, Ont.) · 2023Article
- Enhancer of zeste homolog 2 promotes renal fibrosis after acute kidney injury by inducing epithelial-mesenchymal transition and activation of M2 macrophage polarization.Cell death & disease · 2023Article
- Relaxin inhibits renal fibrosis and the epithelial-to-mesenchymal transition via the Wnt/β-catenin signaling pathway.Renal failure · 2022Article
- Ion channels as a therapeutic target for renal fibrosis.Frontiers in physiology · 2022Review
- Trimethylamine-N-oxide (TMAO) mediates the crosstalk between the gut microbiota and hepatic vascular niche to alleviate liver fibrosis in nonalcoholic steatohepatitis.Frontiers in immunology · 2022Article
- Clinical significance of P-class pumps in cancer.Oncology letters · 2021Review
- Article
- Inverse agonism at the Na/K-ATPase receptor reverses EMT in prostate cancer cells.The Prostate · 2021Article
- Na/K-ATPase beta1-subunit associates with neuronal growth regulator 1 (NEGR1) to participate in intercellular interactions.BMB reports · 2021Article
- Integrative Transcriptomic, Proteomic and Functional Analysis Reveals ATP1B3 as a Diagnostic and Potential Therapeutic Target in Hepatocellular Carcinoma.Frontiers in immunology · 2021Article
- A Targeted Bioinformatics Assessment of Adrenocortical Carcinoma Reveals Prognostic Implications of GABA System Gene Expression.International journal of molecular sciences · 2020Article
- Exploring the Therapeutic Potential of Membrane Transport Proteins: Focus on Cancer and Chemoresistance.Cancers · 2020Review
- Transient Receptor Potential Channel 6 Knockout Ameliorates Kidney Fibrosis by Inhibition of Epithelial-Mesenchymal Transition.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
Epithelial-to-mesenchymal transition (EMT) is an important developmental process, participates in tissue repair, and occurs during pathologic processes of tumor invasiveness, metastasis, and tissue fibrosis. The molecular mechanisms leading to EMT are poorly understood. Although it is well documented that transforming growth factor (TGF)-beta plays a central role in the induction of EMT, the targets of TGF-beta signaling are poorly defined. We have shown earlier that Na,K-ATPase beta(1)-subunit levels are highly reduced in poorly differentiated kidney carcinoma cells in culture and in patients' tumor samples. In this study, we provide evidence that Na,K-ATPase is a new target of TGF-beta(1)-mediated EMT in renal epithelial cells, a model system used in studies of both cancer progression and fibrosis. We show that following treatment with TGF-beta(1), the surface expression of the beta(1)-subunit of Na,K-ATPase is reduced, before well-characterized EMT markers, and is associated with the acquisition of a mesenchymal phenotype. RNAi-mediated knockdown confirmed the specific involvement of the Na,K-ATPase beta(1)-subunit in the loss of the epithelial phenotype and exogenous overexpression of the Na,K-ATPase beta(1)-subunit attenuated TGF-beta(1)-mediated EMT. We further show that both Na,K-ATPase alpha- and beta-subunit levels are highly reduced in renal fibrotic tissues. These findings reveal for the first time that Na,K-ATPase is a target of TGF-beta(1)-mediated EMT and is associated with the progression of EMT in cancer and fibrosis.
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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.