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10.18632/oncotarget.3843 http://scihub22266oqcxt.onion/10.18632/oncotarget.3843 C4599270!4599270 !25915537     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25915537 &cmd=llinks): Failed to open stream: HTTP request failed! 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Ubiquitin C-terminal hydrolase-L1 increases cancer cell invasion by modulating hydrogen peroxide generated via NADPH oxidase 4 |pdf=|usr=}}{{25915537 }} gab.com Text Ubiquitin C-terminal hydrolase-L1 increases cancer cell invasion by modulating hydrogen peroxide generated via NADPH oxidase 4 JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=25915537 #FOAvip This study explored the role of ubiquitin C-terminal hydrolase-L1 (UCH-L1) in the production of ROS and tumor invasion. UCH-L1 was found to increase cellular ROS levels and promote cell invasion. Silencing UCH-L1, as well as inhibition of H2O2 generation by catalase or by DPI, a NOX inhibitor, suppressed the migration potential of B16F10 cells, indicating that UCH-L1 promotes cell migration by up-regulating H2O2 generation. Silencing NOX4, which generates H2O2, with siRNA eliminated the effect of UCH-L1 on cell migration. On the other hand, NOX4 overexpressed in HeLa cells happens to be ubiquitinated, and NOX4 following deubiquitination by UCH-L1, restored H2O2-generating activity. These in vitro findings are consistent with the results obtained in vivo with catalase (-/-) C57BL/6J mice. When H2O2 and UCH-L1 levels were independently varied in these animals, the former by infecting with H2O2-scavenging adenovirus-catalase, and the latter by overexpressing or silencing UCH-L1, pulmonary metastasis of B16F10 cells overexpressing UCH-L1 increased significantly in catalase (-/-) mice. In contrast, invasion did not increase when UCH-L1 was silenced in the B16F10 cells. These findings indicate that H2O2 levels regulated by UCH-L1 are necessary for cell invasion to occur and demonstrate that UCH-L1 promotes cell invasion by up-regulating H2O2 via deubiquitination of NOX4. Twit Text FOAVip Ubiquitin C-terminal hydrolase-L1 increases cancer cell invasion by modulating hydrogen peroxide generated via NADPH oxidase 4 ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=25915537 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25915537 #FOAvip English Wikipedia <ref>{{Cite pmid|25915537 }}</ref> Ubiquitin C-terminal hydrolase-L1 increases cancer cell invasion by modulating hydrogen peroxide generated via NADPH oxidase 4 #MMPMID25915537 Kim HJ ; Magesh V ; Lee JJ ; Kim S ; Knaus UG ; Lee KJ Oncotarget 2015[Jun]; 6 (18 ): 16287-303 PMID25915537 show ga This study explored the role of ubiquitin C-terminal hydrolase-L1 (UCH-L1) in the production of ROS and tumor invasion. UCH-L1 was found to increase cellular ROS levels and promote cell invasion. Silencing UCH-L1, as well as inhibition of H2O2 generation by catalase or by DPI, a NOX inhibitor, suppressed the migration potential of B16F10 cells, indicating that UCH-L1 promotes cell migration by up-regulating H2O2 generation. Silencing NOX4, which generates H2O2, with siRNA eliminated the effect of UCH-L1 on cell migration. On the other hand, NOX4 overexpressed in HeLa cells happens to be ubiquitinated, and NOX4 following deubiquitination by UCH-L1, restored H2O2-generating activity. These in vitro findings are consistent with the results obtained in vivo with catalase (-/-) C57BL/6J mice. When H2O2 and UCH-L1 levels were independently varied in these animals, the former by infecting with H2O2-scavenging adenovirus-catalase, and the latter by overexpressing or silencing UCH-L1, pulmonary metastasis of B16F10 cells overexpressing UCH-L1 increased significantly in catalase (-/-) mice. In contrast, invasion did not increase when UCH-L1 was silenced in the B16F10 cells. These findings indicate that H2O2 levels regulated by UCH-L1 are necessary for cell invasion to occur and demonstrate that UCH-L1 promotes cell invasion by up-regulating H2O2 via deubiquitination of NOX4. |*Cell Movement [MESH] |Animals [MESH] |Apoptosis [MESH] |Blotting, Western [MESH] |Catalase/*physiology [MESH] |Cell Proliferation [MESH] |HeLa Cells [MESH] |Humans [MESH] |Hydrogen Peroxide/*metabolism [MESH] |Immunoenzyme Techniques [MESH] |Immunoprecipitation [MESH] |Lung Neoplasms/genetics/metabolism/*secondary [MESH] |Male [MESH] |Melanoma, Experimental/genetics/metabolism/*pathology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Nude [MESH] |NADPH Oxidases/genetics/*metabolism [MESH] |Neoplasm Invasiveness [MESH] |Protein Processing, Post-Translational [MESH] |RNA, Messenger/genetics [MESH] |RNA, Small Interfering/genetics [MESH] |Reactive Oxygen Species/metabolism [MESH] |Real-Time Polymerase Chain Reaction [MESH] |Reverse Transcriptase Polymerase Chain Reaction [MESH] |Spectrometry, Mass, Electrospray Ionization [MESH] |Tandem Mass Spectrometry [MESH] |Tumor Cells, Cultured [MESH] |Ubiquitin Thiolesterase/antagonists & inhibitors/genetics/*metabolism [MESH] |Ubiquitin/metabolism [MESH]Ubiquitin C-terminal hydrolase-L1 increases cancer cell invasion by mo(epmc).pdf DeepDyve Pubget Overpricing