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MicroRNA-150 Inhibits Cell Invasion and Migration and Is Downregulated in Human Osteosarcoma.

Authors :
Li X
Chen L
Wang W
Meng FB
Zhao RT
Chen Y
Source :
Cytogenetic and genome research [Cytogenet Genome Res] 2015; Vol. 146 (2), pp. 124-135. Date of Electronic Publication: 2015 Sep 12.
Publication Year :
2015

Abstract

miR-150 expression in osteosarcoma (OS) cell lines and human osteoblast cells was detected, and OS cell models were transfected with exogenous miR-150 to investigate its role in cell proliferation, invasion, and apoptosis. Our results showed that miR-150 expression in OS cells (MG63, Saos-2, SOSP-9607, and U2OS) was significantly lower compared to the osteoblast hFOB1.19 cell line (all p < 0.01). The expression level of miR-150 in MG63 cells that were transfected with exogenous miR-150 mimics was markedly upregulated, while the miR-150 expression level in the inhibitor group was significantly downregulated (both p < 0.01). Similar results were also found in SOSP-9607 cells. Importantly, exogenous miR-150 expression stimulated cell apoptosis and inhibited proliferation, invasion, and migration. A luciferase reporter assay displayed that miR-150 also regulated Sp1 expression by targeting its 3'-UTR, and qRT-PCR and Western blotting showed that elevated levels of miR-150 may reduce Sp1 protein expression. The mRNA and protein levels of Sp1 were upregulated after transfection with a Sp1-expression plasmid and partially reversed the inhibitory effects of miR-150 on cell proliferation, invasion, and metastasis in MG63 and SOSP-9607 cells, as well as promoted cell apoptosis. In conclusion, miR-150 inhibits cell proliferation, invasion, and metastasis and stimulates cell apoptosis by regulating the expression of Sp1. Therefore, miR-150 may be a potential clinical target for the treatment of OS patients.<br /> (© 2015 S. Karger AG, Basel.)

Details

Language :
English
ISSN :
1424-859X
Volume :
146
Issue :
2
Database :
MEDLINE
Journal :
Cytogenetic and genome research
Publication Type :
Academic Journal
Accession number :
26361218
Full Text :
https://doi.org/10.1159/000437379