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10.1080/15548627.2015.1108507 http://scihub22266oqcxt.onion/10.1080/15548627.2015.1108507 C4835194!4835194 !26553592     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26553592 &cmd=llinks): Failed to open stream: HTTP request failed! 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MIR517C inhibits autophagy and the epithelial-to-mesenchymal (-like) transition phenotype in human glioblastoma through KPNA2-dependent disruption of TP53 nuclear translocation |pdf=|usr=}}{{26553592 }} gab.com Text MIR517C inhibits autophagy and the epithelial-to-mesenchymal (-like) transition phenotype in human glioblastoma through KPNA2-dependent disruption of TP53 nuclear translocation JO: Autophagy http://www.kidney.de/pget.php?&tw=1&pmid=26553592 #FOAvip The epithelial-to-mesenchymal (-like) transition (EMT), a crucial embryonic development program, has been linked to the regulation of glioblastoma (GBM) progression and invasion. Here, we investigated the role of MIR517C/miR-517c, which belongs to the C19MC microRNA cluster identified in our preliminary studies, in the pathogenesis of GBM. We found that MIR517C was associated with improved prognosis in patients with GBM. Furthermore, following treatment with the autophagy inducer temozolomide (TMZ) and low glucose (LG), MIR517C degraded KPNA2 (karyopherin alpha 2 [RAG cohort 1, importin alpha 1]) and subsequently disturbed the nuclear translocation of TP53 in the GBM cell line U87 in vitro. Interestingly, this microRNA could inhibit autophagy and reduce cell migration and infiltration in U87 cells harboring wild-type (WT) TP53, but not in U251 cells harboring mutant (MU) TP53. Moreover, the expression of epithelial markers (i.e., CDH13/T-cadherin and CLDN1 [claudin 1]) increased, while the expression of mesenchymal markers (i.e., CDH2/N-cadherin, SNAI1/Snail, and VIM [vimentin]) decreased, indicating that the EMT status was blocked by MIR517C in U87 cells. Compared with MIR517C overexpression, MIR517C knockdown promoted infiltration of U87 cells to the surrounding structures in nude mice in vivo. The above phenotypic changes were also observed in TP53(+/+) and TP53(-/-) HCT116 colon cancer cells. In summary, our study provided support for a link between autophagy and EMT status in WT TP53 GBM cells and provided evidence for the signaling pathway (MIR517C-KPNA2-cytoplasmic TP53) involved in attenuating autophagy and eliminating the increased migration and invasion during the EMT. Twit Text FOAVip MIR517C inhibits autophagy and the epithelial-to-mesenchymal (-like) transition phenotype in human glioblastoma through KPNA2-dependent disruption of TP53 nuclear translocation ????Autophagy http://www.kidney.de/pget.php?&tw=1&pmid=26553592 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26553592 #FOAvip English Wikipedia <ref>{{Cite pmid|26553592 }}</ref> MIR517C inhibits autophagy and the epithelial-to-mesenchymal (-like) transition phenotype in human glioblastoma through KPNA2-dependent disruption of TP53 nuclear translocation #MMPMID26553592 Lu Y ; Xiao L ; Liu Y ; Wang H ; Li H ; Zhou Q ; Pan J ; Lei B ; Huang A ; Qi S Autophagy 2015[]; 11 (12 ): 2213-32 PMID26553592 show ga The epithelial-to-mesenchymal (-like) transition (EMT), a crucial embryonic development program, has been linked to the regulation of glioblastoma (GBM) progression and invasion. Here, we investigated the role of MIR517C/miR-517c, which belongs to the C19MC microRNA cluster identified in our preliminary studies, in the pathogenesis of GBM. We found that MIR517C was associated with improved prognosis in patients with GBM. Furthermore, following treatment with the autophagy inducer temozolomide (TMZ) and low glucose (LG), MIR517C degraded KPNA2 (karyopherin alpha 2 [RAG cohort 1, importin alpha 1]) and subsequently disturbed the nuclear translocation of TP53 in the GBM cell line U87 in vitro. Interestingly, this microRNA could inhibit autophagy and reduce cell migration and infiltration in U87 cells harboring wild-type (WT) TP53, but not in U251 cells harboring mutant (MU) TP53. Moreover, the expression of epithelial markers (i.e., CDH13/T-cadherin and CLDN1 [claudin 1]) increased, while the expression of mesenchymal markers (i.e., CDH2/N-cadherin, SNAI1/Snail, and VIM [vimentin]) decreased, indicating that the EMT status was blocked by MIR517C in U87 cells. Compared with MIR517C overexpression, MIR517C knockdown promoted infiltration of U87 cells to the surrounding structures in nude mice in vivo. The above phenotypic changes were also observed in TP53(+/+) and TP53(-/-) HCT116 colon cancer cells. In summary, our study provided support for a link between autophagy and EMT status in WT TP53 GBM cells and provided evidence for the signaling pathway (MIR517C-KPNA2-cytoplasmic TP53) involved in attenuating autophagy and eliminating the increased migration and invasion during the EMT. |Adult [MESH] |Aged [MESH] |Animals [MESH] |Autophagy/*genetics [MESH] |Cadherins/metabolism [MESH] |Cell Line, Tumor [MESH] |Cell Movement/genetics/physiology [MESH] |Dacarbazine/analogs & derivatives/pharmacology [MESH] |Epithelial-Mesenchymal Transition/physiology [MESH] |Female [MESH] |Gene Expression Regulation, Neoplastic/drug effects/genetics [MESH] |Glioblastoma/*metabolism/pathology [MESH] |Humans [MESH] |Male [MESH] |Mice [MESH] |Mice, Nude [MESH] |MicroRNAs/*metabolism [MESH] |Middle Aged [MESH] |Nuclear Proteins/*metabolism [MESH] |Phenotype [MESH] |Temozolomide [MESH] |Tumor Suppressor Protein p53/*metabolism [MESH]MIR517C inhibits autophagy and the epithelial-to-mesenchymal (-like) t(epmc).pdf DeepDyve Pubget Overpricing