Liang Long, Luo Ying, Li Danyang, Sun Yongchang
Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China.
J Cell Mol Med. 2025 May;29(9):e70596. doi: 10.1111/jcmm.70596.
Existing knowledge regarding the involvement of lncRNA OIP5-AS1 in lung adenocarcinoma (LUAD) development is still incomplete and requires further investigation. Our research aimed to reveal the function of OIP5-AS1 in LUAD. We evaluated the level of OIP5-AS1 and its association with clinicopathological factors in LUAD. The research examined the potential implications of targeting OIP5-AS1 in mitigating the invasive properties of lung cancer cells. A nude mouse xenograft model was utilised to examine tumour growth. We used bioinformatics data and a dual-luciferase reporter assay to study the interactions between OIP5-AS1 and hsa-miR-29b-3p. OIP5-AS1 was significantly overexpressed in LUAD, with a higher level correlating with adverse clinicopathological features. Knockdown of OIP5-AS1 resulted in notable decreases in LUAD cell growth, movement, and aggressive behaviour, accompanied by a decrease in tumour size in vivo. Furthermore, OIP5-AS1 was confirmed to act as a molecular sponge for hsa-miR-29b-3p. The elevated expression of hsa-miR-29b-3p intensified the inhibitory outcomes of OIP5-AS1 knockdown on LUAD cell properties. ZIC5 was experimentally determined to be a direct molecular target of hs-miR-29b-3p, emphasising its integral position in the regulatory interaction. This study reveals a new regulatory route involving OIP5-AS1, hsa-miR-29b-3p and ZIC5 in LUAD pathogenesis. Given its oncogenic traits, OIP5-AS1 presents a promising predictive biomarker and therapeutic target for optimising lung cancer treatment.
关于长链非编码RNA OIP5-AS1参与肺腺癌（LUAD）发生发展的现有知识仍不完整，需要进一步研究。我们的研究旨在揭示OIP5-AS1在LUAD中的功能。我们评估了LUAD中OIP5-AS1的水平及其与临床病理因素的关系。该研究探讨了靶向OIP5-AS1对减轻肺癌细胞侵袭特性的潜在影响。利用裸鼠异种移植模型检测肿瘤生长情况。我们使用生物信息学数据和双荧光素酶报告基因检测来研究OIP5-AS1与hsa-miR-29b-3p之间的相互作用。OIP5-AS1在LUAD中显著过表达，其较高水平与不良临床病理特征相关。敲低OIP5-AS1导致LUAD细胞生长、运动和侵袭性行为显著减少，同时体内肿瘤大小减小。此外，证实OIP5-AS1作为hsa-miR-29b-3p的分子海绵发挥作用。hsa-miR-29b-3p的表达升高增强了OIP5-AS1敲低对LUAD细胞特性的抑制作用。实验确定ZIC5是hs-miR-29b-3p的直接分子靶点，强调了其在调节相互作用中的重要地位。本研究揭示了LUAD发病机制中涉及OIP5-AS1、hsa-miR-29b-3p和ZIC5的新调控途径。鉴于其致癌特性，OIP5-AS1为优化肺癌治疗提供了一个有前景的预测生物标志物和治疗靶点。
