- VernacularTitle:ML210通过调控GPX4介导的铁死亡通路抑制脑胶质瘤细胞的作用
- Author:
Ning TIAN
1
;
Yan-lin JIANG
;
Dong-shan YA
;
Xiao-xia LI
;
Bing GUO
;
Ru-jia LIAO
Author Information
- Publication Type:Journal Article
- Keywords: glioma; ML210; GPX4; ferroptosis; U87 cell lines; molecular docking; genomics
- From: Chinese Pharmacological Bulletin 2025;41(4):686-694
- CountryChina
- Language:Chinese
- Abstract: Aim To study the role and mechanism of ML210 in glioma.Methods The cell viability was detected by CCK8 assay.The percentage of dead cells was detected by SYTOXstaining.The role of ferroptosis-signaling pathway in gliomas was detected bygenomics.Cell proliferation was observed by EdU staining and clone formation assay.Cell migration ability was detec-ted by scratch healing assay.The apoptosis was detec-ted by flow cytometry.Cell mitochondrial function was assesses by JC-1 staining.The mechanism of action of ML210 was detected by molecular docking coupled with immunoblotting assay(Western blot).The levels of ROS,MDA were observed by ELISA.Results Compared with the control group,ML210 treatment dose-dependently decreased glioma cell viability,in-hibited cell proliferation,migration,and increased cell apoptosis and mitochondrial dysfunction,which were reversed by ferroptosis antagonists.Gene microarray screening showed that 688 genes of the ferroptosissig-naling pathway were aberrant and 10 signaling path-ways were altered in gliomas.Molecular docking re-sults showed that ML210 binding to GPX4 significantly inhibited the protein expression level of GPX4 and pro-moted the elevation of ROS and MDA levels.Conclu-sions ML210 produces anti-glioma cells via GPX4-mediated ferroptosis pathway.

