Glioma-derived endothelial cells promote glioma cells migration via extracellular vesicles-mediated transfer of MYO1C

Yuan Tian; Zhixing Wang; Yuxin Wang; Bin Yin; Jiangang Yuan; Boqin Qiang; Wei Han; Xiaozhong Peng

doi:10.1016/j.bbrc.2020.02.017

Glioma-derived endothelial cells promote glioma cells migration via extracellular vesicles-mediated transfer of MYO1C

Biochem Biophys Res Commun. 2020 Feb 18:S0006-291X(20)30283-7. doi: 10.1016/j.bbrc.2020.02.017. Online ahead of print.

Authors

Yuan Tian¹, Zhixing Wang¹, Yuxin Wang¹, Bin Yin¹, Jiangang Yuan¹, Boqin Qiang¹, Wei Han², Xiaozhong Peng³

Affiliations

¹ State Key Laboratory of Medical Molecular Biology, Department of Molecular Biology and Biochemistry, Institute of Basic Medical Sciences, Medical Primate Research Center, Neuroscience Center, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, 100005, China.
² State Key Laboratory of Medical Molecular Biology, Department of Molecular Biology and Biochemistry, Institute of Basic Medical Sciences, Medical Primate Research Center, Neuroscience Center, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, 100005, China. Electronic address: hanwei2012@ibms.pumc.edu.cn.
³ State Key Laboratory of Medical Molecular Biology, Department of Molecular Biology and Biochemistry, Institute of Basic Medical Sciences, Medical Primate Research Center, Neuroscience Center, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, 100005, China; Institute of Medical Biology, Chinese Academy of Medical Sciences, Peking Union Medical College, Kunming, China. Electronic address: pengxiaozhong@pumc.edu.cn.

PMID: 32081419
DOI: 10.1016/j.bbrc.2020.02.017

Abstract

Extracellular vesicles (EV), as the intercellular information transfer molecules which can regulate the tumor microenvironment, promote migration and tumor progression. Previous studies reported that EV from endothelial cells was used to guide the fate and survival of gliomas, but many researches focus on normal human endothelial cells (NhEC) rather than tumor-derived endothelial cells. Our laboratory isolated human endothelial cells from glioma issue (GhEC). We have previously demonstrated that EV from GhEC and NhEC, which both can promote glioma stem cells (GSC) proliferation and tumorsphere formation in vitro and tumourigenicity in vivo by the transfer of CD9. However, NhEC-EV or GhEC-EV could suppress glioma cells (GC) proliferation in vitro. It demonstrates the undifferentiated impact of EV. Here, we first compared GhEC-EV proteins with NhEC-EV (Screening criteria: GhEC-EV/NhEC-EV, FC > 1.5), and obtained 70 differential expression proteins, most of which were associated with invasion and migration. We found that GhEC or GhEC-EV preferred promoting GC migration than treating with NhEC or NhEC-EV. In terms of mechanism, we further revealed that EV-mediated transfer of MYO1C induced glioma cell LN229 migration. Knockdown of MYO1C in GhEC or GhEC-EV suppressed this effect. Overexpression of MYO1C promoted migration on the contrary. MYO1C was also detected in glioma cerebrospinal fluid (CSF), which is more suitable as a liquid biopsy biomarker and contributes to early diagnosis and monitoring in glioma. Our findings provide a new protein-MYO1C in EV to target tumor blood vessels, and bring a new point-cut to the treatment of gliomablastoma (GBM).

Keywords: Endothelial cells; Extracellular vesicles; Glioma; MYO1C; Migration.