Cristazine inhibits HPV-positive cervical cancer cells via inducing caspase-dependent apoptosis
Mi Jeong Jo, Jeong Gyu Kim, Seung Hyun Yoo, Cha Young Kim, Jong-Oh Kim, Gun-Do KimObjective:
To determine whether cristazine inhibits HPV-positive cervical cancer cells and to elucidate its underlying mechanisms.
Methods:
HeLa cells were treated with varying concentrations of cristazine, and cell viability, intracellular ROS, apoptosis, and apoptosis-related gene and protein expression were assessed using WST-1, DCF-DA flow cytometry, Annexin V-FITC/PI staining, quantitative RT-PCR, and Western blotting. Additionally, CaSki and SiHa cells were evaluated in viability assays, with selected ROS and apoptosis measurements performed in CaSki cells.
Results:
After 24 h of treatment, cristazine reduced HeLa cell viability with an IC
50
of 0.223 μM and increased intracellular ROS and apoptotic populations. Caspase inhibition substantially restored viability and reduced apoptosis. Cristazine also increased
Conclusions:
Cristazine suppresses cervical cancer cell growth via coordinated ROS-associated, p53-driven, and caspase-dependent apoptotic signaling, highlighting its potential as a marine-derived anticancer candidate that warrants further investigation.