THE LIPOXYGENASE INHIBITOR ML351 AFFECTS CELL VIABILITY BY REGULATING AUTOPHAGY AND SEMAPHORIN SIGNALING PATHWAYS IN A549 CELLS

Lung cancer is one of the leading causes of cancer-related deaths worldwide, and the inadequacy of current treatment strategies necessitates the investigation of new molecular targets. In this study, the effects of the selective 15-lipoxygenase inhibitor ML351 on cell viability, autophagy, and the Semaphorin-3E (SEMA3E) signaling pathway in A549 lung adenocarcinoma cells were examined. Cell viability was evaluated using the MTT assay, and protein levels of autophagy markers (Beclin-1, LC3, and p62) and SEMA3E were measured using the ELISA method. The findings revealed that ML351 exhibited a dose-dependent cytotoxic effect. The IC₅₀ value was calculated as 92 µM, cell viability fell below 80% in the 20–80 µM range, and was almost completely eliminated at 160 µM (***p