MiR-383 inhibits proliferation, migration and angiogenesis of glioma-exposed endothelial cells in vitro via VEGF-mediated FAK and Src signaling pathways.
Malignant glioma is undoubtedly the most vascularized tumor of central nervous system. Angiogenesis, playing a predominant role in tumor progression, is widely considered as a key point of tumor treatment. The aim of this study was to investigate the potential effects of miR-383 on proliferation, migration, tube formation and angiogenesis of glioma-exposed endothelial cells (GECs) in vitro and to further elucidate its possible molecular mechanisms. The expression of miR-383 in GECs was significantly downregulated compared with that in normal endothelial cells (ECs). Overexpression of miR-383 dramatically inhibited the proliferation, migration, tube formation and spheroid-based angiogenesis of GECs in vitro. Dual-luciferase reporter results demonstrated vascular endothelial growth factor (VEGF) is a target gene of miR-383. Furthermore, overexpression or silencing of either miR-383 or VEGF was performed simultaneously to further clarify that miR-383 inhibited proliferation, migration and angiogenesis of GECs in vitro by targeting VEGF. Finally, VEGF/VEGFR2-mediated FAK and Src signaling pathways might contribute to anti-angiogenesis of GECs. In conclusion, our present study indicated that miR-383 inhibits proliferation, migration and angiogenesis of GECs in vitro via VEGF/VEGFR2-mediated FAK and Src signaling pathways, which would draw growing attention to miR-383c as a potential therapeutical target of glioma.
Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang 110122, People's Republic of China; Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110122, People's Republic of China.
Li-Ni
LN
Zhao
Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang 110122, People's Republic of China; Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110122, People's Republic of China.
Ping
P
Wang
Department of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China; Liaoning Research Center for Translational Medicine in Nervous System Disease, Shenyang 110004, People's Republic of China.
Yun-Hui
YH
Liu
Department of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China; Liaoning Research Center for Translational Medicine in Nervous System Disease, Shenyang 110004, People's Republic of China.
Heng
H
Cai
Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang 110122, People's Republic of China; Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110122, People's Republic of China.
Jun
J
Ma
Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang 110122, People's Republic of China; Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110122, People's Republic of China.
Li-Bo
LB
Liu
Department of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China; Liaoning Research Center for Translational Medicine in Nervous System Disease, Shenyang 110004, People's Republic of China.
Zhuo
Z
Xi
Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang 110122, People's Republic of China; Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110122, People's Republic of China.
Zhi-Qing
ZQ
Li
Department of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China; Liaoning Research Center for Translational Medicine in Nervous System Disease, Shenyang 110004, People's Republic of China.
Xiao-Bai
XB
Liu
Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang 110122, People's Republic of China; Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110122, People's Republic of China. Electronic address: xueyixue888@163.com.
Yi-Xue
YX
Xue
D001483:Base Sequence; D001932:Brain Neoplasms / Q000098:blood supply / Q000235:genetics / Q000473:pathology; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics*; D049109:Cell Proliferation; D015536:Down-Regulation; D042783:Endothelial Cells / Q000378:metabolism*; D051416:Focal Adhesion Protein-Tyrosine Kinases / Q000378:metabolism*; D015972:Gene Expression Regulation, Neoplastic; D005910:Glioma / Q000098:blood supply* / Q000235:genetics / Q000473:pathology*; D006801:Humans; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D009389:Neovascularization, Pathologic / Q000235:genetics; D010766:Phosphorylation; D015398:Signal Transduction; D014162:Transfection; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000378:metabolism; D019061:src-Family Kinases / Q000378:metabolism*
C558685:MIRN383 microRNA, human; D035683:MicroRNAs; D042461:Vascular Endothelial Growth Factor A; D040301:Vascular Endothelial Growth Factor Receptor-2; D051416:Focal Adhesion Protein-Tyrosine Kinases; D019061:src-Family Kinases
Angiogenesis; FAK; Glioma-exposed endothelial cells; MiR-383; Src; VEGF