Objective Oesophageal cancer (EC) is an extremely invasive malignancy, which has bad prognosis that requires safe and effective treatment modalities. Immunotherapy has provided new ideas for the treatment of EC in recent years. This project was conducted to probe into the role and mechanism of lncRNA OIP5-AS1 in ferroptosis and immunotherapy of EC. Methods Cell viability and multiplication were assessed through CCK-8, colony formation assays. Levels of Fe2+, MDA, and lipid ROS were applied to determine ferroptosis. GPX4 and OIP5-AS1 levels were examined through real-time PCR assay. The relationship between OIP5-AS1 and GPX4 was estimated through RNA immunoprecipitation assay. Flow cytometry was applied to examine the effect of OIP5-AS1 on CD8+ T cells. Results OIP5-AS1 inhibition significantly inhibited EC cell viability and proliferation, induced ferroptosis, and downregulated GPX4 levels, while GPX4 reversed these effects. OIP5-AS1/GPX4 induced CD8+ T cell interaction and induced apoptosis through PD-1/PD-L1 immune checkpoints of CD8+ T cells. Conclusion OIP5-AS1/GPX4 promotes EC development and relieved ferroptosis; furthermore, OIP5-AS1/GPX4 facilitated immune evasion via modulation of PD-1/PD-L1, suggesting aiming at OIP5-AS1 is a possible route which might enhance the effectiveness of immunotherapy.
