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http://purl.uniprot.org/citations/31829261http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31829261http://www.w3.org/2000/01/rdf-schema#comment"

Background

Accumulating evidence indicates that aberrant microRNA (miRNA) expression contributes to osteosarcoma progression. This study aimed to elucidate the association between miR-624-5p expression and osteosarcoma (OS) development and to investigate its underlying mechanism.

Methods

We analyzed GSE65071 from the GEO database and found miR-624-5p was the most upregulated miRNA. The expression of miR-624-5p and its specific target gene were determined in human OS specimens and cell lines by RT-PCR and western blot. The effects of miR-624-5p depletion or ectopic expression on OS proliferation, migration and invasion were evaluated in vitro using CCK-8 proliferation assay, colony formation assay, transwell assay, would-healing assay and 3D spheroid BME cell invasion assay respectively. We investigated in vivo effects of miR-624-5p using a mouse tumorigenicity model. Besides, luciferase reporter assays were employed to identify interactions between miR-624-5p and its specific target gene.

Results

miR-624-5p expression was upregulated in OS cells and tissues, and overexpressing miR-624-5p led to a higher malignant level of OS, including cell proliferation, migration and invasion in vitro and in vivo. Protein tyrosine phosphatase receptor type B (PTPRB) was negatively correlated with miR-624-5p expression in OS tissues. Using the luciferase reporter assay and Western blotting, PTPRB was confirmed as a downstream target of miR-624-5p. PTPRB restored the effects of miR-624-5p on OS migration and invasion. The Hippo signaling pathway was identified as being involved in the miR-624-5p/PTPRB axis.

Conclusions

In conclusion, our results suggest that miR-624-5p is a negative regulator of PTPRB and a risk factor for tumor metastasis in OS progression."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.org/dc/terms/identifier"doi:10.1186/s13046-019-1491-6"xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Chen J."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Huang Y."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Gong F."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Fan J."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Luo Y."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Gu C."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Liu W."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Wei Y."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Yin G."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Zhao S."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Zhou Z."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Tang P."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Xu T."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Cai W."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Jiang D."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Qian D."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/author"Rong Y."xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/name"J Exp Clin Cancer Res"xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/pages"488"xsd:string
http://purl.uniprot.org/citations/31829261http://purl.uniprot.org/core/title"miR-624-5p promoted tumorigenesis and metastasis by suppressing hippo signaling through targeting PTPRB in osteosarcoma cells."xsd:string
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