WCLC 2025 - Posters & ePosters-P2.02.21 CTNNB1 Activates LINC01426 to Promote Metabolic Reprogramming in Lung Adenocarcinoma Cells by Regulating NFAT5 Nuclear Translocation

P2.02.21 CTNNB1 Activates LINC01426 to Promote Metabolic Reprogramming in Lung Adenocarcinoma Cells by Regulating NFAT5 Nuclear Translocation

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This study investigates the role of CTNNB1 and LINC01426 in lung adenocarcinoma (LUAD) progression, focusing on metabolic reprogramming mechanisms. LUAD, often diagnosed at advanced stages with poor prognosis, involves complex molecular changes. The researchers identified LINC01426, a long non-coding RNA, as significantly upregulated in LUAD tissues through analysis of GEO and TCGA-LUAD databases. Tissue microarray analysis showed higher LINC01426 expression correlated with lower patient survival rates.<br /><br />Mechanistically, CTNNB1 was found to transcriptionally activate LINC01426 by directly binding to its promoter. LINC01426, in turn, interacts with NFAT5 in the cytoplasm, facilitating NFAT5’s translocation into the nucleus. This nuclear translocation of NFAT5 promotes metabolic reprogramming, specifically enhancing glycolysis in LUAD cells, which supports tumor growth and malignancy. Functional experiments demonstrated that knocking down either LINC01426 or NFAT5 suppressed this metabolic shift and inhibited cancer cell proliferation.<br /><br />The study employed bioinformatics tools such as the TFBS R package and JASPAR for transcription factor binding site prediction, R Corr package for gene correlation analysis, and KEGG enrichment to identify relevant pathways. These analyses were complemented by experimental validations confirming LINC01426’s oncogenic role through glycolytic regulation mediated by NFAT5.<br /><br />In summary, CTNNB1 activates LINC01426 expression, which promotes NFAT5 nuclear translocation, triggering metabolic changes that accelerate LUAD progression. This newly elucidated pathway highlights LINC01426 as a potential biomarker and therapeutic target. Future research is suggested to further explore the detailed molecular mechanisms of this regulatory axis in LUAD.<br /><br />The research was supported by the Natural Science Foundation of Shanghai and Tongji University’s Independent Basic Research Project.

Asset Subtitle

Qiyu Fang

Meta Tag

Speaker Qiyu Fang

Topic Tumor Biology – Preclinical Biology

Keywords

CTNNB1

LINC01426

lung adenocarcinoma

LUAD progression

metabolic reprogramming

NFAT5 nuclear translocation

glycolysis enhancement

oncogenic biomarker

transcription factor binding

bioinformatics analysis