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NFATc4 Promotes Lung Adenocarcinoma Progression via the CCNB1/CDK1 Pathway and Is a Potential Prognostic Biomarker
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NFATc4 Promotes Lung Adenocarcinoma Progression via the CCNB1/CDK1 Pathway and Is a Potential Prognostic Biomarker
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Journal Article
NFATc4 Promotes Lung Adenocarcinoma Progression via the CCNB1/CDK1 Pathway and Is a Potential Prognostic Biomarker
2025
Overview
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.
NFATc4 is upregulated in LUAD, and its high expression correlates with the malignant progression of patients. NFATc4 enhances LUAD cell viability and proliferation by regulating the G2/M phase transition and apoptosis. Functionally, NFATc4 directly binds to the CCNB1 promoter, modulating the CCNB1/CDK1 pathway, which results in cell cycle arrest and inhibition of cell proliferation.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc
Subject
/ Adenocarcinoma of Lung - genetics
/ Adenocarcinoma of Lung - metabolism
/ Adenocarcinoma of Lung - mortality
/ Adenocarcinoma of Lung - pathology
/ Animals
/ Biomarkers, Tumor - genetics
/ Biomarkers, Tumor - metabolism
/ CDC2 Protein Kinase - genetics
/ CDC2 Protein Kinase - metabolism
/ CDK1
/ Cell Proliferation - genetics
/ Female
/ Gene Expression Regulation, Neoplastic
/ Genes
/ Humans
/ Kinases
/ Male
/ Mice
/ NFATC Transcription Factors - genetics
/ NFATC Transcription Factors - metabolism
/ nuclear factor of activated T‐cells cytoplasmic 4
/ Original
/ Plasmids
/ Software
/ T cells
