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http://purl.uniprot.org/citations/29542173http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29542173http://www.w3.org/2000/01/rdf-schema#comment"

Background

Our study was aimed at detecting the expression levels of miR-206 in prostate cancer (PCa) tissues and PCa cell lines, and exploring the potential functions of miR-206 by targeting chemokine ligand 11 (CXCL11).

Methods

RT-qPCR was applied to detect the expressions of miR-206 and CXCL11 in PCa tissues and in PCa cell lines. Expression of the CXCL11 protein was detected using Western blot. After manipulating the expression of miR-206 and CXCL11 in PC-3 and DU-145 cells, the changes of cell proliferation and cell cycle were observed through cell counting kit-8 (CCK-8) and flow cytometry. Wound healing and transwell assay were conducted for cell migration and invasion examination in vitro. The luciferase reporter assay was applied to validate the association between miR-206 and CXCL11.

Results

MiR-206 was significantly under-expressed in PCa tissues and in PCa cell lines. Up-regulation of miR-206 could inhibit proliferation, migration, invasion and induced G1/G0 arrest of PCa cells, and vice versa. MiR-206 bound to the 3'-UTR of CXCL11 and significantly repressed the luciferase activity. Overexpression of miR-206 decreased the expression level of CXCL11 significantly. CXCL11 mRNA and protein levels were significantly decreased in PCa cells. Downregulation of CXCL11 presented tumor-suppressing effects on PCa cells as miR-206 mimics did. And co-transfection miR-206 attenuated the tumor-promoting effects induced by CXCL11 overexpression.

Conclusion

Our current finding demonstrated that miR-206 negatively regulated PCa cell proliferation and migration, and arrested cell cycle by targeting CXCL11 as a tumor suppressor in prostate cancer."xsd:string
http://purl.uniprot.org/citations/29542173http://purl.org/dc/terms/identifier"doi:10.1002/pros.23468"xsd:string
http://purl.uniprot.org/citations/29542173http://purl.uniprot.org/core/author"Li Q."xsd:string
http://purl.uniprot.org/citations/29542173http://purl.uniprot.org/core/author"Wang Y."xsd:string
http://purl.uniprot.org/citations/29542173http://purl.uniprot.org/core/author"Xu H."xsd:string
http://purl.uniprot.org/citations/29542173http://purl.uniprot.org/core/author"Zhu X."xsd:string
http://purl.uniprot.org/citations/29542173http://purl.uniprot.org/core/author"Yu T."xsd:string
http://purl.uniprot.org/citations/29542173http://purl.uniprot.org/core/author"Si L."xsd:string
http://purl.uniprot.org/citations/29542173http://purl.uniprot.org/core/author"Gang X."xsd:string
http://purl.uniprot.org/citations/29542173http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/29542173http://purl.uniprot.org/core/name"Prostate"xsd:string
http://purl.uniprot.org/citations/29542173http://purl.uniprot.org/core/pages"479-490"xsd:string
http://purl.uniprot.org/citations/29542173http://purl.uniprot.org/core/title"MiR-206 inhibits proliferation and migration of prostate cancer cells by targeting CXCL11."xsd:string
http://purl.uniprot.org/citations/29542173http://purl.uniprot.org/core/volume"78"xsd:string
http://purl.uniprot.org/citations/29542173http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/29542173
http://purl.uniprot.org/citations/29542173http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/29542173
http://purl.uniprot.org/uniprot/#_O14625-mappedCitation-29542173http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29542173
http://purl.uniprot.org/uniprot/#_Q96KF0-mappedCitation-29542173http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29542173
http://purl.uniprot.org/uniprot/Q96KF0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/29542173
http://purl.uniprot.org/uniprot/O14625http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/29542173