Lycorine inhibits cell proliferation and induced oxidative stress-mediated apoptosis via regulation of the JAK/STAT3 signaling pathway in HT-3 cells

Human cervical cancer is the fourth most common carcinoma in women in the world. The JAK/STAT3 signaling pathways crucially regulate cell growth and apoptosis. It is a significant target signaling pathway for the development of novel antitumor medicine. This study intended to explore whether lycorine could prevent HT-3 proliferation and induce apoptosis by targeting the JAK/STAT3 signaling cascade. The HT-3 cells were treated with various lycorine dosages and we analyzed cell growth, lipid peroxidation, antioxidants, mitochondrial membrane potential (Delta psi m), DNA damage, apoptosis markers by different in vitro methodologies. Our results revealed that lycorine substantially reserved cell growth via decreased antioxidants, augmented reactive oxygen species (ROS) generation which leads to loss of Delta psi m, increased nuclear crumbling and chromatin condensation, thus resulting in representative increased apoptotic cell death. Furthermore, we analyzed that the molecular mechanical action of lycorine considerably repressed JAK1/STAT3 transactional activation and decrease its downstream molecules Bcl-2, and enhances the expressional activity of Bax, cytochrome c, caspase 3 and 9 in HT-3 cells. Finally, the fact that N-acetylcysteine inhibits lycorine-induced ROS-mediated apoptosis was confirmed in HT-3 cells. Thus, the results indicate that lycorine efficiently enhances apoptosis and inhibits HT-3 cell proliferation. These outcomes collectively proposed that lycorine could be a beneficial chemotherapeutic agent for treating and managing human cervical carcinoma.