ArticleJournal of applied genetics2026
DDX11-AS1 regulates cell cycle signaling pathway and promotes proliferation and migration of lung adenocarcinoma by sponging miR-30a-5p and targeting CCNA2.
Article in Journal of applied genetics, 2026. 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
Various long noncoding RNAs (lncRNAs) have a crucial part in treating lung adenocarcinoma (LUAD). However, there are few studies on lncRNA DDX11-AS1 in LUAD. We systematically elucidated its potential molecular mechanism in LUAD, which provides a theoretical basis for studying targeted therapy for LUAD. We have analyzed RNA expression in LUAD through TCGA-LUAD data. The binding site (…CAAAUGU…) was predicted by TargetScan database. Associated pathways were predicted by GSEA database. RT-qPCR to analyze RNA level and western blot to analyze protein abundance. Besides, CCK-8, EdU, Transwell and flow cytometry assays were performed to verify how DDX11-AS1, miR-30a-5p and CCNA2 affected LUAD cells. Targeted relationship was verified by dual luciferase reporter and RIP assays. The role of DDX11-AS1 in vivo was tested by a mouse model and immunohistochemistry. Compared with normal lung tissues or cells, LUAD tissues or cells had higher DDX11-AS1 expression and CCNA2 but lower miR-30a-5p expression. Proliferative, invasive and migratory abilities of LUAD cells could be enhanced by DDX11-AS1, which could further regulate cell cycle changes and attenuate apoptosis. MiR-30a-5p could be targeted and down-regulated by DDX11-AS1, which activated cell cycle signaling pathway through miR-30a-5p/CCNA2 axis. DDX11-AS1 promoted tumor growth in mice. Our research demonstrates that DDX11-AS1, through miR-30a-5p/CCNA2 axis, has a cancer-promotive part in LUAD development. It is suggested that DDX11-AS1 may be a new biomarker and therapeutic target in diagnosing and treating LUAD.
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