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MicroRNA‑640 promotes cell proliferation and adhesion in glioblastoma by targeting Slit guidance ligand 1
Author(s) -
Chao Luo,
Zhiying Lu,
Yongli Chen,
Xiaozhen Chen,
Na Liu,
Jing Chen,
Shanwu Dong
Publication year - 2020
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2020.12422
Subject(s) - microrna , cell growth , cancer research , cell adhesion , cell cycle , oncogene , viability assay , cell , microbiology and biotechnology , chemistry , biology , gene , biochemistry
The effects of microRNAs (miRNAs/miRs) on glioblastoma have attracted the attention of researchers in the last 7 years. However, the role of miR-640 and its targeted gene, Slit guidance ligand 1 (SLIT1), in the development of glioblastoma are not yet fully understood. The present study aimed to investigate the role of miR-640 in the proliferation and adhesion of glioblastoma. Reverse transcription-quantitative PCR analysis was performed to detect miR-640 and SLIT1 expression in glioblastoma tissues and cells. In addition, the Dual-luciferase reporter and RNA-pull down assays were performed to assess the association between miR-640 and SLIT1. The Cell Counting Kit-8, BrdU ELISA, cell adhesion and caspase-3 activity assays were also performed to assess cell viability, proliferation, adhesion and apoptosis of glioblastoma cells, respectively. The results demonstrated that miR-640 expression was upregulated in glioblastoma tissues and cells. In addition, miR-640 promoted the cell viability, proliferation and adhesion of glioblastoma cells, while inhibiting cell apoptosis. SLIT1, a direct downstream target of miR-640, was demonstrated to be downregulated in glioblastoma tissues and cells. Furthermore, overexpression of SLIT1 attenuated the promotive effect of miR-640 on glioblastoma cells. Taken together, these results suggest that miR-640 accelerates the proliferation and adhesion of glioblastoma cell lines by targeting and suppressing SLIT1.

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