@article{jfnr202513123,
author={{Kim, Seon-Hee and Lee, Dong Seok},
title={<i>Orostachys Japonicus</i> Promotes Apoptosis in Cervical Cancer Cells through Modulation of NF-¦ªB and ERK1/2 Pathways},
journal={Journal of Food and Nutrition Research},
volume={13},
number={12},
pages={455--461},
year={2025},
url={https://pubs.sciepub.com/jfnr/13/12/3},
issn={2333-1240},
abstract={Cervical cancer remains a significant global health burden, necessitating the development of safer and more effective therapeutic agents. <i>Orostachys japonicus</i>, a traditional medicinal herb, has shown promising anti-cancer activity, but its molecular mechanisms in cervical cancer cells have not been fully elucidated. We investigated the pro-apoptotic effects of the ethyl acetate fraction of <i>O. japonicus</i> (E-OJ) on HeLa cells and compared its activity to known phenolic constituents (kaempferol, quercetin, and gallic acid). Apoptosis was assessed by Annexin V/PI flow cytometry and DAPI staining. Western blot analysis was used to examine NF-¦ÊB and MAPK signaling pathways, as well as caspase-3 activation. The role of ERK signaling was further evaluated using the ERK-specific inhibitor U0126. E-OJ treatment induced significant, dose-dependent apoptosis in HeLa cells, accompanied by nuclear fragmentation and chromatin condensation. Compared to individual compounds, E-OJ exhibited greater apoptotic efficacy. Mechanistically, E-OJ suppressed NF-¦ÊB signaling by blocking nuclear translocation of the NF-¦ÊB p65 subunit. Among the MAPK pathways, only ERK1/2 was activated by E-OJ. Inhibition of ERK1/2 with U0126 attenuated caspase-3 cleavage, indicating that ERK signaling mediates E-OJ-induced apoptosis through a caspase-3-dependent mechanism. These findings suggest that E-OJ induces apoptosis in cervical cancer cells by suppressing NF-¦ÊB activation and promoting ERK1/2-mediated caspase-3 activation. The superior efficacy of E-OJ compared to its individual phenolic components highlights its therapeutic potential as a natural anti-cancer agent.},
doi={10.12691/jfnr-13-12-3}
publisher={Science and Education Publishing}
}
