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


PARLAK M., JOHA Z., YULAK F., Mendil A. S., TAŞTEMUR Y.

Journal of Receptors and Signal Transduction, 2024 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Basım Tarihi: 2024
  • Doi Numarası: 10.1080/10799893.2024.2426516
  • Dergi Adı: Journal of Receptors and Signal Transduction
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, Chemical Abstracts Core, MEDLINE
  • Anahtar Kelimeler: Anticancer, apoptosis, autophagy, lycopene
  • Sivas Cumhuriyet Üniversitesi Adresli: Evet

Özet

Background: 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 LC3β (autophagy) and 8-oxo-dG (DNA damage). Results: Lycopene significantly killed HeLa cells in a dose-dependent way (IC50 = 10 μM). 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 LC3β 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.