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10.18632/oncotarget.5105 http://scihub22266oqcxt.onion/10.18632/oncotarget.5105 C4741615!4741615 !26429879     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26429879 &cmd=llinks): Failed to open stream: HTTP request failed! 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Extracellular vesicle-mediated transfer of CLIC1 protein is a novel mechanism for the regulation of glioblastoma growth |pdf=|usr=}}{{26429879 }} gab.com Text Extracellular vesicle-mediated transfer of CLIC1 protein is a novel mechanism for the regulation of glioblastoma growth JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26429879 #FOAvip Little progresses have been made in the treatment of glioblastoma (GBM), the most aggressive and lethal among brain tumors. Recently we have demonstrated that Chloride Intracellular Channel-1 (CLIC1) is overexpressed in GBM compared to normal tissues, with highest expression in patients with poor prognosis. Moreover, CLIC1-silencing in cancer stem cells (CSCs) isolated from human GBM patients negatively influences proliferative capacity and self-renewal properties in vitro and impairs the in vivo tumorigenic potential. Here we show that CLIC1 exists also as a circulating protein, secreted via extracellular vesicles (EVs) released by either cell lines or GBM-derived CSCs. Extracellular vesicles (EVs), comprising exosomes and microvesicles based on their composition and biophysical properties, have been shown to sustain tumor growth in a variety of model systems, including GBM. Interestingly, treatment of GBM cells with CLIC1-containing EVs stimulates cell growth both in vitro and in vivo in a CLIC1-dose dependent manner. EVs derived from CLIC1-overexpressing GBM cells are strong inducers of proliferation in vitro and tumor engraftment in vivo. These stimulations are significantly attenuated by treatment of GBM cells with EVs derived from CLIC1-silenced cells. However, CLIC1 modulation appears to have no direct role in EV structure, biogenesis and secretion. These findings reveal that, apart from the function of CLIC1 cellular reservoir, CLIC1 contained in EVs is a novel regulator of GBM growth. Twit Text FOAVip Extracellular vesicle-mediated transfer of CLIC1 protein is a novel mechanism for the regulation of glioblastoma growth ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26429879 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26429879 #FOAvip English Wikipedia <ref>{{Cite pmid|26429879 }}</ref> Extracellular vesicle-mediated transfer of CLIC1 protein is a novel mechanism for the regulation of glioblastoma growth #MMPMID26429879 Setti M ; Osti D ; Richichi C ; Ortensi B ; Del Bene M ; Fornasari L ; Beznoussenko G ; Mironov A ; Rappa G ; Cuomo A ; Faretta M ; Bonaldi T ; Lorico A ; Pelicci G Oncotarget 2015[Oct]; 6 (31 ): 31413-27 PMID26429879 show ga Little progresses have been made in the treatment of glioblastoma (GBM), the most aggressive and lethal among brain tumors. Recently we have demonstrated that Chloride Intracellular Channel-1 (CLIC1) is overexpressed in GBM compared to normal tissues, with highest expression in patients with poor prognosis. Moreover, CLIC1-silencing in cancer stem cells (CSCs) isolated from human GBM patients negatively influences proliferative capacity and self-renewal properties in vitro and impairs the in vivo tumorigenic potential. Here we show that CLIC1 exists also as a circulating protein, secreted via extracellular vesicles (EVs) released by either cell lines or GBM-derived CSCs. Extracellular vesicles (EVs), comprising exosomes and microvesicles based on their composition and biophysical properties, have been shown to sustain tumor growth in a variety of model systems, including GBM. Interestingly, treatment of GBM cells with CLIC1-containing EVs stimulates cell growth both in vitro and in vivo in a CLIC1-dose dependent manner. EVs derived from CLIC1-overexpressing GBM cells are strong inducers of proliferation in vitro and tumor engraftment in vivo. These stimulations are significantly attenuated by treatment of GBM cells with EVs derived from CLIC1-silenced cells. However, CLIC1 modulation appears to have no direct role in EV structure, biogenesis and secretion. These findings reveal that, apart from the function of CLIC1 cellular reservoir, CLIC1 contained in EVs is a novel regulator of GBM growth. |Animals [MESH] |Apoptosis [MESH] |Blotting, Western [MESH] |Brain Neoplasms/metabolism/*pathology [MESH] |Cell Proliferation [MESH] |Chloride Channels/*metabolism [MESH] |Exosomes/metabolism/*pathology [MESH] |Extracellular Vesicles/metabolism/*pathology [MESH] |Glioblastoma/metabolism/*pathology [MESH] |Humans [MESH] |Immunoenzyme Techniques [MESH] |Mice [MESH] |Mice, Nude [MESH] |Nanoparticles/chemistry [MESH] |Neoplastic Stem Cells/metabolism/*pathology [MESH] |Tumor Cells, Cultured [MESH]Extracellular vesicle-mediated transfer of CLIC1 protein is a novel me(epmc).pdf DeepDyve Pubget Overpricing