ArticleTranslational cancer research2025
LINC01314 suppresses proliferation and invasion via epithelial-to-mesenchymal transition regulation in lung adenocarcinoma.
Article in Translational cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Long intergenic non-protein coding RNA 1314 (LINC01314) is significantly downregulated in lung adenocarcinoma; however, its functional role in tumor progression remains unclear. We investigated the impact of LINC01314 on lung adenocarcinoma aggressiveness and explored the underlying mechanisms. Methods: Expression levels of LINC01314 and its association with clinicopathological features and patient survival were evaluated using The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Results: LINC01314 was markedly under-expressed in lung adenocarcinoma tissues. Reduced LINC01314 levels were correlated with advanced pathological stage and poorer overall survival. Functionally, LINC01314 knockdown enhanced, whereas its overexpression suppressed, cell proliferation, migration, and invasion. GSEA consistently revealed that low LINC01314 expression was associated with upregulation of epithelial-to-mesenchymal transition (EMT) pathways. Furthermore, western blot analysis revealed that LINC01314 knockdown resulted in a decrease in epithelial markers (E-cadherin and ZO-1) and an increase in mesenchymal markers (vimentin) and matrix metalloproteinases (MMP2, and MMP9); conversely, overexpression reversed these expression patterns. Conclusions: These findings suggest that LINC01314 functions as a tumor suppressor in lung adenocarcinoma by modulating EMT-related pathways. LINC01314 holds promise as both a prognostic biomarker and a potential therapeutic target in lung adenocarcinoma.
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