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10.18632/oncotarget.14465 http://scihub22266oqcxt.onion/10.18632/oncotarget.14465 C5386699!5386699 !28061448     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28061448 &cmd=llinks): Failed to open stream: HTTP request failed! 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Targeting basal-like breast tumors with bromodomain and extraterminal domain (BET) and polo-like kinase inhibitors |pdf=|usr=}}{{28061448 }} gab.com Text Targeting basal-like breast tumors with bromodomain and extraterminal domain (BET) and polo-like kinase inhibitors JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28061448 #FOAvip Metastatic triple negative breast cancer (TNBC) is an incurable disease with limited therapeutic options, and no targeted therapies available. Triple negative tumors and the basal-like genomic subtype, are both characterized by a high proliferation rate and an increase in cell division. In this context, protein kinases involved in the mitotic formation have a relevant role in this tumor subtype. Recently, Bromodomain and extraterminal domain (BET) inhibitors have shown to be active in this disease by modulating the expression of several transcription factors. In this article, by using an "in silico" approach, we identified genomic functions that can be inhibited pharmacologically in basal-like tumors. Functional annotation analyses identified "cell division" and "regulation of transcription" as upregulated functions. When focus on cell division, we identified the polo-like kinase 1 (PLK) as an upregulated kinase. The PLK inhibitor Volasertib had the strongest anti-proliferative effect compared with other inhibitors against mitotic kinases. Gene expression analyses demonstrated that the BET inhibitor JQ1 reduced the expression of kinases involved in cell division, and synergized with Volasertib in a panel of triple negative cell lines. Combination of both agents augmented cell death. Similarly, combination of both compounds reduced the expression of stem cell markers. Globally, this data demonstrates the synergistic interaction between BET and PLK inhibitors, paving the way for their future clinical development. Twit Text FOAVip Targeting basal-like breast tumors with bromodomain and extraterminal domain (BET) and polo-like kinase inhibitors ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28061448 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28061448 #FOAvip English Wikipedia <ref>{{Cite pmid|28061448 }}</ref> Targeting basal-like breast tumors with bromodomain and extraterminal domain (BET) and polo-like kinase inhibitors #MMPMID28061448 Nieto-Jiménez C ; Alcaraz-Sanabria A ; Pérez-Peña J ; Corrales-Sánchez V ; Serrano-Heras G ; Galán-Moya EM ; Serrano-Oviedo L ; Montero JC ; Burgos M ; Llopis J ; Pandiella A ; Ocaña A Oncotarget 2017[Mar]; 8 (12 ): 19478-19490 PMID28061448 show ga Metastatic triple negative breast cancer (TNBC) is an incurable disease with limited therapeutic options, and no targeted therapies available. Triple negative tumors and the basal-like genomic subtype, are both characterized by a high proliferation rate and an increase in cell division. In this context, protein kinases involved in the mitotic formation have a relevant role in this tumor subtype. Recently, Bromodomain and extraterminal domain (BET) inhibitors have shown to be active in this disease by modulating the expression of several transcription factors. In this article, by using an "in silico" approach, we identified genomic functions that can be inhibited pharmacologically in basal-like tumors. Functional annotation analyses identified "cell division" and "regulation of transcription" as upregulated functions. When focus on cell division, we identified the polo-like kinase 1 (PLK) as an upregulated kinase. The PLK inhibitor Volasertib had the strongest anti-proliferative effect compared with other inhibitors against mitotic kinases. Gene expression analyses demonstrated that the BET inhibitor JQ1 reduced the expression of kinases involved in cell division, and synergized with Volasertib in a panel of triple negative cell lines. Combination of both agents augmented cell death. Similarly, combination of both compounds reduced the expression of stem cell markers. Globally, this data demonstrates the synergistic interaction between BET and PLK inhibitors, paving the way for their future clinical development. |Apoptosis/drug effects [MESH] |Biomarkers, Tumor/*metabolism [MESH] |Breast Neoplasms/*drug therapy/metabolism/pathology [MESH] |Carcinoma, Basal Cell/*drug therapy/metabolism/pathology [MESH] |Cell Cycle Proteins/*antagonists & inhibitors [MESH] |Cell Proliferation/drug effects [MESH] |Female [MESH] |Histone Acetyltransferases [MESH] |Histone Chaperones [MESH] |Humans [MESH] |Neoplasm Invasiveness [MESH] |Nuclear Proteins/*antagonists & inhibitors [MESH] |Polo-Like Kinase 1 [MESH] |Protein Kinase Inhibitors/*pharmacology [MESH] |Protein Serine-Threonine Kinases/*antagonists & inhibitors [MESH] |Proto-Oncogene Proteins/*antagonists & inhibitors [MESH]Targeting basal-like breast tumors with bromodomain and extraterminal (epmc).pdf DeepDyve Pubget Overpricing