ArticleFrontiers in physiology2014
NFAT5-mediated expression of S100A4 contributes to proliferation and migration of renal carcinoma cells.
Article in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed.
- The effects of telmisartan on the nuclear factor of activated T lymphocytes signalling pathway in hypertensive patients.Journal of the renin-angiotensin-aldosterone system : JRAASTrial
- Unlocking the therapeutic potential of the NFAT pathway in kidney diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Hyperosmolar stress induces monocyte chemoattractant protein 1 expression in retinal pigmented epithelial arising retinal pigmented epithelial 19 cells.Molecular vision · 2025Article
- High salt-induced osmotic stress differentially modulates hepatocellular and renal carcinoma cell proliferation.Frontiers in oncology · 2025Article
- HES1 potentiates high salt stress response as an enhancer of NFAT5-DNA binding.Communications biology · 2024Article
- TonEBP/NFAT5 expression is associated with cisplatin resistance and migration in macrophage-induced A549 cells.BMC molecular and cell biology · 2024Article
- Serum amyloid A expression in liver promotes synovial macrophage activation and chronic arthritis via NFAT5.The Journal of clinical investigation · 2024Article
- ROCK2-RNA interaction map reveals multiple biological mechanisms underlying tumor progression in renal cell carcinoma.Human cell · 2023Article
- SAFB2 Inhibits the Progression of Breast Cancer by Suppressing the Wnt/β-Catenin Signaling Pathway via NFAT5.Molecular biotechnology · 2023Article
- Article
- Dialog beyond the Grave: Necrosis in the Tumor Microenvironment and Its Contribution to Tumor Growth.International journal of molecular sciences · 2023Review
- FSP-1 expression in cancer cells is relevant to long-term oncological outcomes in nonmetastatic colorectal cancer.Korean journal of clinical oncology · 2022Article
- Circular RNA_0037128 aggravates high glucose-induced damage in HK-2 cells via regulation of microRNA-497-5p/nuclear factor of activated T cells 5 axis.Bioengineered · 2021Article
- CD40 Cross-Linking Induces Migration of Renal Tumor Cell through Nuclear Factor of Activated T Cells (NFAT) Activation.International journal of molecular sciences · 2021Article
- Article
- NFAT5 Regulated by STUB1, Facilitates Malignant Cell Survival and p38 MAPK Activation by Upregulating AQP5 in Chronic Lymphocytic Leukemia.Biochemical genetics · 2021Article
- Pathogenic mechanisms and the potential clinical value of circFoxo3 in cancers.Molecular therapy. Nucleic acids · 2021Review
- The Role of Artificial Intelligence in the Diagnosis and Prognosis of Renal Cell Tumors.Diagnostics (Basel, Switzerland) · 2021Review
- Expression, Prognosis and Gene Regulation Network of NFAT Transcription Factors in Non-Small Cell Lung Cancer.Pathology oncology research : POR · 2021Article
- Effect of shRNA-mediated regulation of S100A4 gene expression on proliferation and apoptosis of KLE endometrial cancer cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021Article
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3 authors.
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No grant is acknowledged in the PubMed record.
Abstract
The osmosensitive transcription factor nuclear factor of activated T-cells (NFAT) 5, also known as tonicity enhancer binding protein (TonEBP), has been associated with the development of a variety of tumor entities, among them breast cancer, colon carcinoma, and melanoma. The aim of the present study was to determine whether NFAT5 is also involved in the development of renal cell carcinoma (RCC). The most common type of RCC, the clear cell RCC, originates from the proximal convoluted tubule. We tested our hypothesis in the clear cell RCC cell line CaKi-1 and the non-cancerous proximal tubule cell line HK-2, as control. Basal expression of NFAT5 and NFAT5 activity in CaKi-1 cells was several times higher than in HK-2 cells. Osmotic stress induced an increased NFAT5 activity in both CaKi-1 and HK-2 cells, again with significantly higher activities in CaKi-1 cells. Analysis of NFAT5-regulating signaling pathways in CaKi-1 cells revealed that inhibition of the MAP kinases p38, c-Jun-terminal kinase (JNK) and extracellular regulated kinase (ERK) and of the focal adhesion kinase (FAK) partially blunted NFAT5 activity. FAK and ERK were both constitutively active, even under isotonic conditions, which may contribute to the high basal expression and activity of NFAT5 in CaKi-1 cells. In contrast, the MAP kinases p38 and JNK were inactive under isotonic conditions and became activated under osmotic stress conditions, indicating that p38 and JNK mediate upregulation of NFAT5 activity under these conditions. siRNA-mediated knockdown of NFAT5 in CaKi-1 cells reduced the expression of S100A4, a member of the S100 family of proteins, which promotes metastasis. Knockdown of NFAT5 was accompanied by a significant decrease in proliferation and migration activity. Taken together, our results indicate that NFAT5 induces S100A4 expression in CaKi-1 cells, thereby playing an important role in RCC proliferation and migration.
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