Dual targeting agent Thiotert inhibits the progression of glioblastoma by inducing ER stress-dependent autophagy

  • Impact factors: 7.5
  • Publication: BIOMEDICINE & PHARMACOTHERAPY
  • Author:Jianhong Dong, Yiming Qian, Wei Zhang, Qian Wang, Mengxian Jia, Juanqing Yue, Ziwei Fan, Yuanyuan Jiang, Lipei Wang, Yongjie Wang, Zhihui Huang, Lushan Yu, Ying Wang
  • DOI citation-doi:10.1016/j.biopha.2023.115867
  • Date:2023-12-15

Glioblastoma (GBM) is the most aggressive and lethal type of tumor in the central nervous system, characterized by a high incidence and poor prognosis. Thiotert, as a novel dual targeting agent, has potential inhibitory effects on various tumors. Here, we found that Thiotert effectively inhibited the proliferation of GBM cells by inducing G2/M cell cycle arrest and suppressed the migratory ability in vitro. Furthermore, Thiotert disrupted the thioredoxin (Trx) system while causing cellular DNA damage, which in turn caused endoplasmic reticulum (ER) stress-dependent autophagy. Knockdown of ER stress-related protein ATF4 in U251 cells inhibited ER stress-dependent autophagy caused by Thiotert to some extent. Orthotopic transplantation experiments further showed that Thiotert had the same anti-GBM activity and mechanism as in vitro. Conclusively, these results suggest that Thiotert induces ER stress-dependent autophagy in GBM cells by disrupting redox homeostasis and causing DNA damage, which provides new insight for the treatment of GBM.

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