Lycopene induces antiproliferative effects through apoptosis, autophagy, and oxidative DNA damage in the HeLa cells

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dc.authoridJoha, Ziad/0000-0001-8520-3760
dc.contributor.authorParlak, Mesut
dc.contributor.authorJoha, Ziad
dc.contributor.authorYulak, Fatih
dc.contributor.authorMendil, Ali Sefa
dc.contributor.authorTastemur, Yasar
dc.date.accessioned2025-05-04T16:46:55Z
dc.date.available2025-05-04T16:46:55Z
dc.date.issued2024
dc.departmentSivas Cumhuriyet Üniversitesi
dc.description.abstractBackground: 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.
dc.identifier.doi10.1080/10799893.2024.2426516
dc.identifier.endpage121
dc.identifier.issn1079-9893
dc.identifier.issn1532-4281
dc.identifier.issue3
dc.identifier.pmid39506337
dc.identifier.scopus2-s2.0-85208489695
dc.identifier.scopusqualityQ2
dc.identifier.startpage115
dc.identifier.urihttps://doi.org/10.1080/10799893.2024.2426516
dc.identifier.urihttps://hdl.handle.net/20.500.12418/35405
dc.identifier.volume44
dc.identifier.wosWOS:001350129400001
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherTaylor & Francis Ltd
dc.relation.ispartofJournal of Receptors and Signal Transduction
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WOS_20250504
dc.subjectAnticancer
dc.subjectlycopene
dc.subjectautophagy
dc.subjectapoptosis
dc.titleLycopene induces antiproliferative effects through apoptosis, autophagy, and oxidative DNA damage in the HeLa cells
dc.typeArticle

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