Parlak, MesutJoha, ZiadYulak, FatihMendil, Ali SefaTastemur, Yasar2025-05-042025-05-0420241079-98931532-4281https://doi.org/10.1080/10799893.2024.2426516https://hdl.handle.net/20.500.12418/35405Background: This study explores the role of apoptosis, autophagy, and oxidative DNA damage in influencing the cytotoxic impact of lycopene on HeLa cells. Material and methods: Cell viability following exposure to varying lycopene concentrations was determined using an XTT assay. ELISA measured key cell death proteins (Bax, BCL-2, etc.), while immunofluorescence staining visualized LC3 beta (autophagy) and 8-oxo-dG (DNA damage). Results: Lycopene significantly killed HeLa cells in a dose-dependent way (IC50 = 10 mu M). Subsequent examinations conducted with the IC50 dose of lycopene demonstrated a notable elevation in the expression levels of apoptotic proteins, such as cleaved caspase 3, cleaved PARP, and Bax (p < 0.001). Additionally, treatment with this substance led to an increase in the levels of 8-oxo-dG (p < 0.001), a widely acknowledged biomarker indicative of oxidative DNA damage. Furthermore, a significant rise (p < 0.05) in LC3 beta protein levels, a well-established indicator of autophagy activation, was noted. Conclusion: This study suggests lycopene's potential to fight cervical cancer by triggering programmed cell death (apoptosis) and cellular self-digestion (autophagy). These findings highlight lycopene as a promising candidate for future cervical cancer treatments.en10.1080/10799893.2024.2426516info:eu-repo/semantics/closedAccessAnticancerlycopeneautophagyapoptosisArticle443121115395063372-s2.0-85208489695Q2WOS:001350129400001Q3