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10.1186/s13046-015-0222-x http://scihub22266oqcxt.onion/10.1186/s13046-015-0222-x C4575431!4575431 !26384788     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26384788 &cmd=llinks): Failed to open stream: HTTP request failed! 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Targeted inhibition of MEK1 by cobimetinib leads to differentiation and apoptosis in neuroblastoma cells |pdf=|usr=}}{{26384788 }} gab.com Text Targeted inhibition of MEK1 by cobimetinib leads to differentiation and apoptosis in neuroblastoma cells JO: J Exp Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26384788 #FOAvip BACKGROUND: Neuroblastoma (NB) is one of the most common childhood malignancies. Currently, high risk NB carries a poor outcome and significant treatment related toxicities and, thus has been a focus for new therapeutics research in pediatric oncology. In this study, we evaluated the effects of the MEK inhibitor cobimetinib, as a single agent and in combinations, on the growth, survival and differentiation properties against a molecularly representative panel of NB cell lines. METHODS: In vitro anti-proliferative activity of cobimetinib alone or in combination was investigated by cell viability assays and its target modulatory activity was evaluated using phospho-kinases antibody arrays and western blot analysis. To determine the effect of combination with cis-RA on differentiation and resulting enhanced cellular cytotoxicity, the expression of glial fibrillary acidic protein (GFAP) and microtubule-associated protein 2 (MAP2) expression levels were examined by immuno-fluorescence. RESULTS: Our findings show that cobimetinib alone induced a concentration-dependent loss of cell viability in all NB cell lines. In addition, cobimetinib showed feedback activation of MEK1/2, and the dephosphorylation of extracellular signal-regulated kinases (ERK1/2) and c-RAF, providing information on the biological correlates of MEK inhibition in NB. Combined treatment with cis-RA, led to differentiation and enhanced sensitization of NB cells lines to cobimetinib. CONCLUSION: Collectively, our results provide evidence that cobimetinib, in combination with cis-RA, represents a feasible option to develop novel treatment strategies for refractory NB. Twit Text FOAVip Targeted inhibition of MEK1 by cobimetinib leads to differentiation and apoptosis in neuroblastoma cells ????J Exp Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26384788 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26384788 #FOAvip English Wikipedia <ref>{{Cite pmid|26384788 }}</ref> Targeted inhibition of MEK1 by cobimetinib leads to differentiation and apoptosis in neuroblastoma cells #MMPMID26384788 Singh A ; Ruan Y ; Tippett T ; Narendran A J Exp Clin Cancer Res 2015[Sep]; 34 (1 ): 104 PMID26384788 show ga BACKGROUND: Neuroblastoma (NB) is one of the most common childhood malignancies. Currently, high risk NB carries a poor outcome and significant treatment related toxicities and, thus has been a focus for new therapeutics research in pediatric oncology. In this study, we evaluated the effects of the MEK inhibitor cobimetinib, as a single agent and in combinations, on the growth, survival and differentiation properties against a molecularly representative panel of NB cell lines. METHODS: In vitro anti-proliferative activity of cobimetinib alone or in combination was investigated by cell viability assays and its target modulatory activity was evaluated using phospho-kinases antibody arrays and western blot analysis. To determine the effect of combination with cis-RA on differentiation and resulting enhanced cellular cytotoxicity, the expression of glial fibrillary acidic protein (GFAP) and microtubule-associated protein 2 (MAP2) expression levels were examined by immuno-fluorescence. RESULTS: Our findings show that cobimetinib alone induced a concentration-dependent loss of cell viability in all NB cell lines. In addition, cobimetinib showed feedback activation of MEK1/2, and the dephosphorylation of extracellular signal-regulated kinases (ERK1/2) and c-RAF, providing information on the biological correlates of MEK inhibition in NB. Combined treatment with cis-RA, led to differentiation and enhanced sensitization of NB cells lines to cobimetinib. CONCLUSION: Collectively, our results provide evidence that cobimetinib, in combination with cis-RA, represents a feasible option to develop novel treatment strategies for refractory NB. |Antineoplastic Combined Chemotherapy Protocols/pharmacology [MESH] |Apoptosis/*drug effects [MESH] |Azetidines/*pharmacology [MESH] |Cell Differentiation/*drug effects [MESH] |Cell Line, Tumor [MESH] |Cell Proliferation/drug effects [MESH] |Cell Survival/drug effects [MESH] |Extracellular Signal-Regulated MAP Kinases/metabolism [MESH] |Glial Fibrillary Acidic Protein/biosynthesis [MESH] |Humans [MESH] |Isotretinoin/*pharmacology [MESH] |MAP Kinase Kinase 1/*antagonists & inhibitors [MESH] |MAP Kinase Signaling System/drug effects [MESH] |Microtubule-Associated Proteins/biosynthesis [MESH] |Neuroblastoma/*drug therapy/pathology [MESH] |Piperidines/*pharmacology [MESH]Targeted inhibition of MEK1 by cobimetinib leads to differentiation an(epmc).pdf DeepDyve Pubget Overpricing