• • OSBPL2 overexpression reduced cholesterol content by HPLC-MS quantification, directly linking lipid transport to stemness suppression; this matters clinically because cholesterol-rich membrane microdomains are known to sustain oncogenic signaling, and targeting this axis could overcome therapy resistance in NSCLC.
• • In peritoneal carcinomatosis models, mice injected with L-Osbpl2-transduced LLC cells (5×10^6 cells/100µL, n=10 per group) showed significantly fewer metastatic tumors after 3 weeks compared to L-Vector controls, demonstrating in vivo efficacy; this provides preclinical proof-of-concept for OSBPL2-based intervention against metastasis.
• • OSBPL2 expression negatively correlated with tumor stage progression and lymph node metastasis in clinical specimens, with repression of ALDH1A1, CD133, and Nanog; this positions OSBPL2 as a prognostic biomarker and a potential companion diagnostic for stemness-targeted therapies.
• • Tumor sphere formation and stemness marker expression were significantly suppressed by OSBPL2-mediated lipid transportation, with experiments repeated three times and analyzed by one-way ANOVA or Student’s t-test (means ± s.e.m.); this robustness supports further development of OSBPL2 agonists or lipid-modulating agents as adjuvant treatments.