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10.3892/ol.2017.6488 http://scihub22266oqcxt.onion/10.3892/ol.2017.6488 C5588166!5588166 !28928831     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28928831 &cmd=llinks): Failed to open stream: HTTP request failed! 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PARK2 negatively regulates the metastasis and epithelial-mesenchymal transition of glioblastoma cells via ZEB1 |pdf=|usr=}}{{28928831 }} gab.com Text PARK2 negatively regulates the metastasis and epithelial-mesenchymal transition of glioblastoma cells via ZEB1 JO: Oncol Lett http://www.kidney.de/pget.php?&tw=1&pmid=28928831 #FOAvip Glioblastoma multiforme (GBM), one of the most aggressive human malignant brain tumors, is induced by multiple complex pathological mechanisms. The main cause of mortality in patients with GBM is the invasion-metastasis cascade of tumor cells. The dysfunction of Parkinson protein 2 E3 ubiquitin protein ligase (PARK2) is closely linked with the development of certain human cancers. However, whether PARK2 is associated with metastasis in GBM remains unknown. The present study demonstrated that the metastasis and invasion of U87 cells were significantly repressed by PARK2 overexpression. Conversely, knockdown of PARK2 facilitated the metastasis and invasion of A172 cells. Furthermore, PARK2 downregulated zinc finger E-box-binding homeobox 1 (ZEB1) expression and mitigated epithelial-mesenchymal transition (EMT). Promoter effects of PARK2 knockdown on cell metastasis and EMT were antagonized by silencing ZEB1 expression. These results indicated that PARK2 participated in regulating the invasion-metastasis cascade of cancer cells by depressing ZEB1 expression and acting as a metastasis suppressor in GBM progression, providing a potential therapeutic approach for GBM treatment. Twit Text FOAVip PARK2 negatively regulates the metastasis and epithelial-mesenchymal transition of glioblastoma cells via ZEB1 ????Oncol Lett http://www.kidney.de/pget.php?&tw=1&pmid=28928831 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28928831 #FOAvip English Wikipedia <ref>{{Cite pmid|28928831 }}</ref> PARK2 negatively regulates the metastasis and epithelial-mesenchymal transition of glioblastoma cells via ZEB1 #MMPMID28928831 Wang H ; Jiang Z ; Na M ; Ge H ; Tang C ; Shen H ; Lin Z Oncol Lett 2017[Sep]; 14 (3 ): 2933-2939 PMID28928831 show ga Glioblastoma multiforme (GBM), one of the most aggressive human malignant brain tumors, is induced by multiple complex pathological mechanisms. The main cause of mortality in patients with GBM is the invasion-metastasis cascade of tumor cells. The dysfunction of Parkinson protein 2 E3 ubiquitin protein ligase (PARK2) is closely linked with the development of certain human cancers. However, whether PARK2 is associated with metastasis in GBM remains unknown. The present study demonstrated that the metastasis and invasion of U87 cells were significantly repressed by PARK2 overexpression. Conversely, knockdown of PARK2 facilitated the metastasis and invasion of A172 cells. Furthermore, PARK2 downregulated zinc finger E-box-binding homeobox 1 (ZEB1) expression and mitigated epithelial-mesenchymal transition (EMT). Promoter effects of PARK2 knockdown on cell metastasis and EMT were antagonized by silencing ZEB1 expression. These results indicated that PARK2 participated in regulating the invasion-metastasis cascade of cancer cells by depressing ZEB1 expression and acting as a metastasis suppressor in GBM progression, providing a potential therapeutic approach for GBM treatment. äPARK2 negatively regulates the metastasis and epithelial-mesenchymal t(epmc).pdf DeepDyve Pubget Overpricing