ArticleCancer science2025
NFATc4 Promotes Lung Adenocarcinoma Progression via the CCNB1/CDK1 Pathway and Is a Potential Prognostic Biomarker.
Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Integrative single-cell and spatial transcriptomic analysis reveals a lactate-driven crosstalk between NFATc4⁺ tumor cells and SPP1⁺ macrophages in glioblastoma.Journal of translational medicine · 2026Article
- The flavonoid astragalin induces apoptosis in lung adenocarcinoma and correlates with a prognostic cell cycle gene signature associated with PANoptosis.Translational cancer research · 2026Article
- Integrating network toxicology with multi-omics approaches to elucidate molecular targets and pathway mechanisms in BPA-induced hepatocellular carcinoma.Molecular diversity · 2026Article
- Unraveling heterogeneity in LUAD via multi-omics integration: molecular classification and therapeutic implications.Discover oncology · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
Nuclear factor of activated T-cells, cytoplasmic 4 (NFATc4), a transcription factor of the NFAT family, has been reported to participate in the tumorigenesis and progression of several cancers. However, the function and regulation of NFATc4 in lung adenocarcinoma (LUAD) remain poorly understood. Here, we report for the first time that NFATc4 is significantly overexpressed in LUAD tissues, and high NFATc4 expression correlates with lymphatic metastasis, advanced tumor stage, and poor prognosis in patients. Subsequent functional studies revealed that NFATc4 depletion inhibits LUAD cell viability, proliferation, and tumor growth by inducing cell cycle arrest in the G2/M phase and apoptosis. A mechanistic study shows that NFATc4 knockdown leads to significant enrichment of cellular process-related pathways and differentially expressed genes, especially downregulated genes Cyclin B1 (CCNB1) and cyclin-dependent kinase 1 (CDK1). NFATc4 directly binds to the CCNB1 promoter to regulate the CCNB1/CDK1 pathway, resulting in cell cycle arrest and inhibition of cell proliferation. This study identifies NFATc4/CCNB1/CDK1 as a novel regulatory pathway involved in LUAD development and provides a potential prognostic biomarker and molecular therapeutic target for LUAD.
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