[This retracts the article DOI: 10.3389/fnmol.2017.00208.].
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http://dx.doi.org/10.3389/fnmol.2024.1543503 | DOI Listing |
Front Mol Neurosci
December 2024
[This retracts the article DOI: 10.3389/fnmol.2017.
View Article and Find Full Text PDFFront Mol Neurosci
June 2017
Department of Neurobiology, College of Basic Medicine, China Medical UniversityShenyang, China.
The obstacle in delivering therapeutics to glioblastoma (GBM) is tumor-induced angiogenesis which leads to the formation of abnormal vessels and a dysfunctional blood-tumor barrier. Here, we elucidated the effect of endothelial-monocyte activating polypeptide II (EMAP II) on the GBM-induced angiogenesis as well as its potential mechanisms. Our results proved that EMAP II inhibited the viability, mitochondrial membrane potential, migration and tube formation of GBM-induced endothelial cells (GECs) by inducing cell autophagy, demonstrated by cell viability assay, JC-1 staining assay, transwell assay and tube formation assay, respectively.
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