LNC511 inhibits lung cancer progression by modulating the miR-625/LOXL4/Wnt/β-catenin pathway.

Lung cancer (LC) is a major contributor to cancer-related deaths worldwide, and long noncoding RNAs (lncRNAs) play significant roles in cancer progression. This study focused on the lncRNA LNC511 and its impact on LC cell activity. Through microarray analysis, we identified differentially expressed lncRNAs in LC tissues, revealing that LNC511 was significantly downregulated in both LC tissues and cell lines. We employed reverse transcription quantitative polymerase chain reaction (RT-qPCR) to measure LNC511 expression levels and performed functional assays to evaluate the effects of LNC511 overexpression on the proliferation, viability, migration, invasion, apoptosis, and stemness of H1299 and A549 cells. Our findings demonstrated that overexpression of LNC511 inhibited these cellular processes. Notably, LNC511 was predominantly localized in the cytoplasm and acted as a molecular sponge for miR-625, leading to the upregulation of LOXL4 and inactivation of the Wnt/β-catenin signaling pathway. The inhibitory effects of LNC511 on LC were reversed by either overexpressing miR-625 or downregulating LOXL4, while a specific agonist of the Wnt/β-catenin pathway also negated these effects. In conclusion, LNC511 inhibits LC cell proliferation and stemness by sponging miR-625, promoting LOXL4 expression and consequently inactivating the Wnt/β-catenin signaling pathway.