| http://purl.uniprot.org/citations/23208072 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23208072 | http://www.w3.org/2000/01/rdf-schema#comment | "Background/aimsOver the past decade, heat shock protein 90 (Hsp90) has emerged as a potential therapeutic target for cancer. However, the molecular mechanisms of down-regulation Hsp90 expression in osteosarcoma are incompletely understood. To develop potential therapy targeting Heat shock protein 90B1 (Hsp90B1), we studied the roles of miR-223 in the proliferation and apoptosis of human osteosarcoma.MethodspcDNA3.1(+)-miR-223 plasmid vectors were constructed and transfected into MG63 cells. Co-transfection of miR-223 expression vector with pMIR-Hsp90B1 (The recombined vector of pMIR-GLOTM luciferase vector containing Hsp90B1-3'UTR) led to the reduced activity of luciferase in a dual-luciferase reporter gene assay, suggesting that Hsp90B1 is a target gene of miR-223. Expression of HSP90B1 was detected by RT-PCR and western blotting analysis. Cell proliferation was determined using the MTT assay. Cell-cycle distribution and apoptosis were examined by flow cytometry. PI3K, p-Akt, Akt, mTOR, Bcl-2 and Bid were also detected by western blotting analysis. After a mouse xenograft model of human MG63 tumors was constructed, tumor growth, microvessel density and proliferation in each group was determined.ResultsThe pcDNA3.1(+)-miR-223 vector efficiently suppressed the expression of HSP90B1, while silencing miR-223 increased expression of Hsp90B1. Furthermore, overexpression of miR-223 results in significant inhibition of cell growth on culture plates. Moreover, cancer cells showed significant G0/G1 arrest and increased apoptosis due to gene silencing. Protein levels of PI3k, p-Akt, mTOR, and Bcl-2 were decreased, whereas Bid levels were increased. Microvessel density as assessed by CD34 levels and cell growth by PCNA levels decreased according to immunohistochemical analysis.ConclusionHsp90B1 is a direct target of miR-223 and miR-223 may have a tumor suppressor function in osteosarcoma through the PI3K/Akt/mTOR pathway and could be used in anticancer therapies in osteosarcoma."xsd:string |
| http://purl.uniprot.org/citations/23208072 | http://purl.org/dc/terms/identifier | "doi:10.1159/000343336"xsd:string |
| http://purl.uniprot.org/citations/23208072 | http://purl.uniprot.org/core/author | "Cai Z."xsd:string |
| http://purl.uniprot.org/citations/23208072 | http://purl.uniprot.org/core/author | "Li G."xsd:string |
| http://purl.uniprot.org/citations/23208072 | http://purl.uniprot.org/core/author | "Sun M."xsd:string |
| http://purl.uniprot.org/citations/23208072 | http://purl.uniprot.org/core/author | "Chen K."xsd:string |
| http://purl.uniprot.org/citations/23208072 | http://purl.uniprot.org/core/author | "Cheng B."xsd:string |
| http://purl.uniprot.org/citations/23208072 | http://purl.uniprot.org/core/author | "Fu D."xsd:string |
| http://purl.uniprot.org/citations/23208072 | http://purl.uniprot.org/core/author | "Cai M."xsd:string |
| http://purl.uniprot.org/citations/23208072 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/23208072 | http://purl.uniprot.org/core/name | "Cell Physiol Biochem"xsd:string |
| http://purl.uniprot.org/citations/23208072 | http://purl.uniprot.org/core/pages | "1481-1490"xsd:string |
| http://purl.uniprot.org/citations/23208072 | http://purl.uniprot.org/core/title | "Heat shock protein 90B1 plays an oncogenic role and is a target of microRNA-223 in human osteosarcoma."xsd:string |
| http://purl.uniprot.org/citations/23208072 | http://purl.uniprot.org/core/volume | "30"xsd:string |
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