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10.1158/1535-7163.MCT-15-1018 http://scihub22266oqcxt.onion/10.1158/1535-7163.MCT-15-1018 C4936950!4936950 !27196781     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27196781 &cmd=llinks): Failed to open stream: HTTP request failed! 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PIM Kinase Inhibitors Kill Hypoxic Tumor Cells by Reducing Nrf2 Signaling and Increasing Reactive Oxygen Species |pdf=|usr=}}{{27196781 }} gab.com Text PIM Kinase Inhibitors Kill Hypoxic Tumor Cells by Reducing Nrf2 Signaling and Increasing Reactive Oxygen Species JO: Mol Cancer Ther http://www.kidney.de/pget.php?&tw=1&pmid=27196781 #FOAvip Intratumoral hypoxia is a significant obstacle to the successful treatment of solid tumors, and it is highly correlated with metastasis, therapeutic resistance, and disease recurrence in cancer patients. As a result, there is an urgent need to develop effective therapies that target hypoxic cells within the tumor microenvironment. The Proviral Integration site for Moloney murine leukemia virus (PIM) kinases represent a prosurvival pathway that is upregulated in response to hypoxia, in a HIF-1-independent manner. We demonstrate that pharmacologic or genetic inhibition of PIM kinases is significantly more toxic toward cancer cells in hypoxia as compared with normoxia. Xenograft studies confirm that PIM kinase inhibitors impede tumor growth and selectively kill hypoxic tumor cells in vivo Experiments show that PIM kinases enhance the ability of tumor cells to adapt to hypoxia-induced oxidative stress by increasing the nuclear localization and activity of nuclear factor-erythroid 2 p45-related factor 2 (Nrf2), which functions to increase the expression of antioxidant genes. Small molecule PIM kinase inhibitors prevent Nrf2 from accumulating in the nucleus, reducing the transcription of cytoprotective genes and leading to the build-up of intracellular reactive oxygen species (ROS) to toxic levels in hypoxic tumor cells. This toxic effect of PIM inhibitors can be successfully blocked by ROS scavengers, including N-acetyl cystine and superoxide dismutase. Thus, inhibition of PIM kinases has the potential to oppose hypoxia-mediated therapeutic resistance and induce cell death in the hypoxic tumor microenvironment. Mol Cancer Ther; 15(7); 1637-47. ©2016 AACR. Twit Text FOAVip PIM Kinase Inhibitors Kill Hypoxic Tumor Cells by Reducing Nrf2 Signaling and Increasing Reactive Oxygen Species ????Mol Cancer Ther http://www.kidney.de/pget.php?&tw=1&pmid=27196781 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27196781 #FOAvip English Wikipedia <ref>{{Cite pmid|27196781 }}</ref> PIM Kinase Inhibitors Kill Hypoxic Tumor Cells by Reducing Nrf2 Signaling and Increasing Reactive Oxygen Species #MMPMID27196781 Warfel NA ; Sainz AG ; Song JH ; Kraft AS Mol Cancer Ther 2016[Jul]; 15 (7 ): 1637-47 PMID27196781 show ga Intratumoral hypoxia is a significant obstacle to the successful treatment of solid tumors, and it is highly correlated with metastasis, therapeutic resistance, and disease recurrence in cancer patients. As a result, there is an urgent need to develop effective therapies that target hypoxic cells within the tumor microenvironment. The Proviral Integration site for Moloney murine leukemia virus (PIM) kinases represent a prosurvival pathway that is upregulated in response to hypoxia, in a HIF-1-independent manner. We demonstrate that pharmacologic or genetic inhibition of PIM kinases is significantly more toxic toward cancer cells in hypoxia as compared with normoxia. Xenograft studies confirm that PIM kinase inhibitors impede tumor growth and selectively kill hypoxic tumor cells in vivo Experiments show that PIM kinases enhance the ability of tumor cells to adapt to hypoxia-induced oxidative stress by increasing the nuclear localization and activity of nuclear factor-erythroid 2 p45-related factor 2 (Nrf2), which functions to increase the expression of antioxidant genes. Small molecule PIM kinase inhibitors prevent Nrf2 from accumulating in the nucleus, reducing the transcription of cytoprotective genes and leading to the build-up of intracellular reactive oxygen species (ROS) to toxic levels in hypoxic tumor cells. This toxic effect of PIM inhibitors can be successfully blocked by ROS scavengers, including N-acetyl cystine and superoxide dismutase. Thus, inhibition of PIM kinases has the potential to oppose hypoxia-mediated therapeutic resistance and induce cell death in the hypoxic tumor microenvironment. Mol Cancer Ther; 15(7); 1637-47. ©2016 AACR. |Animals [MESH] |Biphenyl Compounds/pharmacology [MESH] |Cell Line, Tumor [MESH] |Cell Proliferation/drug effects [MESH] |Cell Survival/drug effects [MESH] |Disease Models, Animal [MESH] |Humans [MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/genetics/metabolism [MESH] |Hypoxia/genetics/*metabolism [MESH] |Male [MESH] |Mice [MESH] |Models, Biological [MESH] |NF-E2-Related Factor 2/*metabolism [MESH] |Neoplasms/drug therapy/genetics/*metabolism/pathology [MESH] |Prostatic Neoplasms/drug therapy/genetics/metabolism/pathology [MESH] |Protein Binding [MESH] |Protein Kinase Inhibitors/*pharmacology [MESH] |Protein Transport [MESH] |Proto-Oncogene Proteins c-pim-1/*antagonists & inhibitors [MESH] |Reactive Oxygen Species/*metabolism [MESH] |Signal Transduction/*drug effects [MESH] |Thiazolidines/pharmacology [MESH]PIM Kinase Inhibitors Kill Hypoxic Tumor Cells by Reducing Nrf2 Signal(epmc).pdf DeepDyve Pubget Overpricing