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<p>Glioma is a common malignant tumor in nervous system, but the treatment efficacy is still unsatisfactory. Licochalcone A (Lic-A) is a kind of flavonoid isolated from glycyrrhiza and shows anti-tumor effect. This study aimed to investigate anti-tumor efficacy of Lic-A on glioma using both in vivo and in vitro models. The in vitro results showed that Lic-A inhibited the growth, migration, and invasion of glioma cells in a dose-dependent way. Lic-A induced mitochondrial dysfunction by regulating Bcl-2 family and induced reactive oxygen species (ROS), while ROS inhibition enhanced the migration and invasion of glioma cells. Finally, animal experiments confirmed that Lic-A inhibited the growth of glioma in vivo. In conclusion, our results suggest that Lic-A can inhibit the migration and invasion of glioma cells while inducing apoptosis of glioma cells. The mechanism may be related to the activation of ATM/ATR pathway and the induction of oxidative stress.</p>

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Licochalcone A inhibits glioma migration, invasion, and growth by triggering mitochondrial dysfunction and ROS-mediated oxidative damage

  • 期刊论文

  • 发表日期：

    2025年8月6日

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  • Chao Yu,
  • Deyan Yang,
  • Nannan Li,
  • Xiaotong Feng,
  • Qile Song,
  • Fusen Zhang,
  • Yuyang Fu,
  • Ping Li

摘要

Glioma is a common malignant tumor in nervous system, but the treatment efficacy is still unsatisfactory. Licochalcone A (Lic-A) is a kind of flavonoid isolated from glycyrrhiza and shows anti-tumor effect. This study aimed to investigate anti-tumor efficacy of Lic-A on glioma using both in vivo and in vitro models. The in vitro results showed that Lic-A inhibited the growth, migration, and invasion of glioma cells in a dose-dependent way. Lic-A induced mitochondrial dysfunction by regulating Bcl-2 family and induced reactive oxygen species (ROS), while ROS inhibition enhanced the migration and invasion of glioma cells. Finally, animal experiments confirmed that Lic-A inhibited the growth of glioma in vivo. In conclusion, our results suggest that Lic-A can inhibit the migration and invasion of glioma cells while inducing apoptosis of glioma cells. The mechanism may be related to the activation of ATM/ATR pathway and the induction of oxidative stress.