The prognosis for non-small cell lung cancer (NSCLC) remains poor, and its underlying molecular mechanisms require further elucidation. This study aimed to systematically investigate the clinical significance, biological function, and potential molecular mechanism of long non‑coding RNA OTX2-AS1 in NSCLC. OTX2-AS1 expression was examined in a clinical cohort comprising 111 NSCLC patients, and its correlation with clinicopathological characteristics and prognosis was analyzed. OTX2-AS1 expression was modulated in cancer cells via transfection, and its impact on malignant behaviors was assessed using cell counting kit‑8, Transwell, and flow cytometry assays. The direct interactions within the OTX2-AS1/miR-377-5p/eukaryotic translation initiation factor 5A2 (EIF5A2) axis were verified by dual-luciferase reporter and RNA immunoprecipitation experiments. OTX2-AS1 was significantly upregulated in NSCLC tissues and cell lines. Its elevated expression independently correlated with unfavorable patient prognosis. In vitro functional assays confirmed that OTX2-AS1 knockdown inhibited cell viability and invasion while promoting apoptosis in NSCLC cells. Mechanistically, OTX2-AS1 functioned as a molecular sponge to directly sequester miR-377-5p, which in turn targeted and regulated the oncogene EIF5A2. Inhibiting miR-377-5p reversed the anti-tumor effects induced by OTX2-AS1 knockdown, whereas silencing EIF5A2 counteracted the tumor-promoting effects of miR-377-5p inhibition. Activation of this axis upregulated EIF5A2, subsequently suppressing E-cadherin and promoting N-cadherin expression. This study suggests that OTX2-AS1 may promote NSCLC progression by sponging miR-377-5p, leading to EIF5A2upregulation and potential induction of epithelial‑mesenchymal transition. The OTX2-AS1/miR-377-5p/EIF5A2 axis may serve as a potential prognostic biomarker and therapeutic target for NSCLC.
Song et al. (Sat,) studied this question.