Arenobufagin, isolated from Bufo viridis toad venom, inhibits A549 cells proliferation by inducing apoptosis and G2/M cell cycle arrest

• Published in: Toxicon (Oxford) 2024-03, Vol.240, p.107641-107641, Article 107641
• Main Authors: Dong, Qiang, Turdu, Gulmira, Akber Aisa, Haji, Yili, Abulimiti
• Format: Article
• Language: English
• Subjects: Apoptosis; Arenobufagin; Bufotes viridis; cancer therapy; Cell cycle; cell cycle checkpoints; cell growth; Cytotoxic effect; cytotoxicity; lung neoplasms; mortality; neoplasm cells; reactive oxygen species; ROS; toad venoms
• ISSN: 0041-0101; 1879-3150
• DOI: 10.1016/j.toxicon.2024.107641

Lung cancer is a significant contributor to cancer morbidity and mortality globally. Arenobufagin, a compound derived from Bufo viridis toad venom, has demonstrated the ability to inhibit cell growth in various cancer cell lines. However, our understanding of the role and mechanism of arenobufagin in lung cancer remains incomplete, necessitating further researches to fully elucidate its action mechanism. In this study, we further explored the impact of arenobufagin on A549 cells. The results revealed that it exerted a potent cytotoxic effect on A549 cells by inhibiting cell colony formation, promoting cell apoptosis, increasing reactive oxygen species (ROS) levels, and arresting A549 cells in G2/M phase. Collectively, our findings suggested that arenobufagin may have potential as a future therapeutic for lung cancer treatment. [Display omitted] •It is the first study that arenobufagin inhibits the cell cycle in A549 cells.•The mechanism of cytotoxicity of arenobufagin was discussed.•Arenobufagin exhibited significant cytotoxic activity with notable selectivity.