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<p>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.</p>

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DDX11-AS1 regulates cell cycle signaling pathway and promotes proliferation and migration of lung adenocarcinoma by sponging miR-30a-5p and targeting CCNA2

  • 期刊论文

  • 发表日期：

    2026年4月17日

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  • Chuanqin Xu,
  • Bo Ai

摘要

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.