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

Toxicon. 2024 Mar:240:107641. doi: 10.1016/j.toxicon.2024.107641. Epub 2024 Feb 7.

Abstract

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.

Keywords: Apoptosis; Arenobufagin; Cell cycle; Cytotoxic effect; ROS.

MeSH terms

  • A549 Cells
  • Amphibian Venoms* / pharmacology
  • Apoptosis
  • Bufanolides*
  • Cell Cycle Checkpoints
  • Cell Line, Tumor
  • Cell Proliferation
  • G2 Phase Cell Cycle Checkpoints
  • Humans
  • Lung Neoplasms* / drug therapy
  • Reactive Oxygen Species / metabolism

Substances

  • arenobufagin
  • Amphibian Venoms
  • Reactive Oxygen Species
  • Bufanolides