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http://purl.uniprot.org/citations/26845432http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26845432http://www.w3.org/2000/01/rdf-schema#comment"

Background

Multiple myeloma (MM), a clonal B cell malignancy characterized by the proliferation of plasma cells within the bone marrow, is still an incurable disease, and therefore, finding new therapeutic targets is urgently required. Although microRNA-137 (miR-137), which is involved in a variety of cellular processes, has been reported to be under-expressed in many types of solid tumors, its role in MM is less known.

Methods

In this study, the target gene and the potential effect of miR-137 in MM were investigated. .

Results

The results showed significantly down regulated expression of miR-137 in MM cell lines and in the CD138+ bone marrow mononuclear cells of MM patients. A dual luciferase reporter gene analysis revealed that MITF is a direct target of miR-137. The overexpression of miR-137 or transfection of MITF-shRNA had no significant effect on the expression of serine/ threonine protein kinase (AKT), but the expression of MITF, c-MET, p-AKT, and its phosphorylated substrate protein decreased significantly, which was accompanied by an increase in p53 expression. In addition, the overexpression of miR-137 or MITF-shRNA significantly improved the 36-hour inhibition rate and apoptosis rate in multiple myeloma cells treated with dexamethasone. The overexpression of MITF could counteract the biological effect of miR-137 in multiple myeloma cells.

Conclusion

We conclude that MITF is a direct target of miR-137. The miR-137 can improve the dexamethasone sensitivity in multiple myeloma cells by reducing the c-MET expression and further decreasing the AKT phosphorylation via targeting MITF."xsd:string
http://purl.uniprot.org/citations/26845432http://purl.org/dc/terms/identifier"doi:10.2174/1568009616666160203114140"xsd:string
http://purl.uniprot.org/citations/26845432http://purl.uniprot.org/core/author"Chen Y."xsd:string
http://purl.uniprot.org/citations/26845432http://purl.uniprot.org/core/author"Hu J."xsd:string
http://purl.uniprot.org/citations/26845432http://purl.uniprot.org/core/author"Ma L."xsd:string
http://purl.uniprot.org/citations/26845432http://purl.uniprot.org/core/author"Wang Y."xsd:string
http://purl.uniprot.org/citations/26845432http://purl.uniprot.org/core/author"Zhang B."xsd:string
http://purl.uniprot.org/citations/26845432http://purl.uniprot.org/core/author"Zhao Z."xsd:string
http://purl.uniprot.org/citations/26845432http://purl.uniprot.org/core/author"Wei J."xsd:string
http://purl.uniprot.org/citations/26845432http://purl.uniprot.org/core/author"Zhao F."xsd:string
http://purl.uniprot.org/citations/26845432http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/26845432http://purl.uniprot.org/core/name"Curr Cancer Drug Targets"xsd:string
http://purl.uniprot.org/citations/26845432http://purl.uniprot.org/core/pages"807-817"xsd:string
http://purl.uniprot.org/citations/26845432http://purl.uniprot.org/core/title"miR-137 Suppresses the Phosphorylation of AKT and Improves the Dexamethasone Sensitivity in Multiple Myeloma Cells Via Targeting MITF."xsd:string
http://purl.uniprot.org/citations/26845432http://purl.uniprot.org/core/volume"16"xsd:string
http://purl.uniprot.org/citations/26845432http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/26845432
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