Study on the molecular mechanism of chlorotoxin from Buthus martensii Karsch in the inhibition of glioma angiogenesis
4 affiliations
- 1Department of Neurosurgery, Heyou Hospital, Foshan, China.
- 2Department of Neurosurgery, Shanxi Provincial People's Hospital, Taiyuan, China.
- 3Department of Neurosurgery, Xi'an International Medical Center Hospital, Xian, China.
- 4Department of Neurosurgery, Wenzhou Hospital of Integrated Traditional Chinese and Western Medicine affiliated to Zhejiang Chinese Medical University, Wenzhou, China.
Abstract
Background: Glioma is a highly malignant intracranial tumor with dismal prognosis. Tumor angiogenesis critically drives glioma growth and invasion, making vascular endothelial cells a promising therapeutic target. Buthus martensii Karsch chlorotoxin (BmK CT) presents favorable antitumor properties, whereas its regulatory role in glioma angiogenesis and the specific mechanism remain poorly defined. Aim: To investigate the regulatory role of BmK CT in glioma angiogenesis and the underlying mechanism. Methods: HUVECs were cultured alone or exposed to glioma conditioned medium prepared from primary glioma cells. Functional assays were performed to assess the impacts of BmK CT on endothelial proliferation, migration and tube formation. Quantitative proteomics and bioinformatics analysis were applied to screen differentially expressed proteins (DEPs) and explore underlying mechanisms. Results: BmK CT significantly inhibited the proliferation of HUVEC cells and reduced their migration and tube formation abilities. BmK CT reversed the promoting effect of primary glioma cells on the migration of HUVEC cells. Proteomics identified multiple DEPs. Enrichment analysis suggested that BmK CT exerts an anti-glioma angiogenesis effect through a multi-target mechanism by inhibiting pro-angiogenic pathways, blocking energy metabolism, and regulating the inflammatory microenvironment. Furthermore, expression pattern clustering analysis revealed six DEPs expression patterns. Parallel reaction monitoring (PRM) analysis supported nine candidate proteins (THBS1, THBS4, COMP, F2, A2M, C3, RIGI, EZR, and ITGA6) associated with glioma angiogenesis. Conclusion: This study demonstrated in vitro that BmK CT inhibits endothelial angiogenic behaviors relevant to glioma progression and modulates the tumor microenvironment, and identified nine candidate DEPs, providing a theoretical basis for future molecular targeted therapy strategies for glioma.
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BibTeX
@article{wang2026study,
title = {{Study on the molecular mechanism of chlorotoxin from Buthus martensii Karsch in the inhibition of glioma angiogenesis}},
author = {Yiming Wang and Yaning Zhao and Ziyang Ren and Yiran Chen and Liangchong Chen and Tao Hu},
journal = {PLOS One},
year = {2026},
month = oct,
doi = {10.1371/journal.pone.0361186},
url = {https://doi.org/10.1371/journal.pone.0361186},
note = {CC BY},
}
RIS
TY - JOUR
TI - Study on the molecular mechanism of chlorotoxin from Buthus martensii Karsch in the inhibition of glioma angiogenesis
AU - Yiming Wang
AU - Yaning Zhao
AU - Ziyang Ren
AU - Yiran Chen
AU - Liangchong Chen
AU - Tao Hu
PY - 2026
DA - 2026/10/29
JO - PLOS One
DO - 10.1371/journal.pone.0361186
UR - https://doi.org/10.1371/journal.pone.0361186
AB - Background: Glioma is a highly malignant intracranial tumor with dismal prognosis. Tumor angiogenesis critically drives glioma growth and invasion, making vascular endothelial cells a promising therapeutic target. Buthus martensii Karsch chlorotoxin (BmK CT) presents favorable antitumor properties, whereas its regulatory role in glioma angiogenesis and the specific mechanism remain poorly defined. Aim: To investigate the regulatory role of BmK CT in glioma angiogenesis and the underlying mechanism. Methods: HUVECs were cultured alone or exposed to glioma conditioned medium prepared from primary glioma cells. Functional assays were performed to assess the impacts of BmK CT on endothelial proliferation, migration and tube formation. Quantitative proteomics and bioinformatics analysis were applied to screen differentially expressed proteins (DEPs) and explore underlying mechanisms. Results: BmK CT significantly inhibited the proliferation of HUVEC cells and reduced their migration and tube formation abilities. BmK CT reversed the promoting effect of primary glioma cells on the migration of HUVEC cells. Proteomics identified multiple DEPs. Enrichment analysis suggested that BmK CT exerts an anti-glioma angiogenesis effect through a multi-target mechanism by inhibiting pro-angiogenic pathways, blocking energy metabolism, and regulating the inflammatory microenvironment. Furthermore, expression pattern clustering analysis revealed six DEPs expression patterns. Parallel reaction monitoring (PRM) analysis supported nine candidate proteins (THBS1, THBS4, COMP, F2, A2M, C3, RIGI, EZR, and ITGA6) associated with glioma angiogenesis. Conclusion: This study demonstrated in vitro that BmK CT inhibits endothelial angiogenic behaviors relevant to glioma progression and modulates the tumor microenvironment, and identified nine candidate DEPs, providing a theoretical basis for future molecular targeted therapy strategies for glioma.
SN - 1932-6203
ER -