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10.1038/cddis.2017.235 http://scihub22266oqcxt.onion/10.1038/cddis.2017.235 C5520894!5520894 !28569777     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28569777 &cmd=llinks): Failed to open stream: HTTP request failed! 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The novel hypoxia-inducible factor-1? inhibitor IDF-11774 regulates cancer metabolism, thereby suppressing tumor growth |pdf=|usr=}}{{28569777 }} gab.com Text The novel hypoxia-inducible factor-1 inhibitor IDF-11774 regulates cancer metabolism, thereby suppressing tumor growth JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28569777 #FOAvip HIF-1 is associated with poor prognoses and therapeutic resistance in cancer patients. We previously developed a novel hypoxia-inducible factor (HIF)-1 inhibitor, IDF-11774, a clinical candidate for cancer therapy. We also reported that IDF-1174 inhibited HSP70 chaperone activity and suppressed accumulation of HIF-1?. In this study, IDF-11774 inhibited the accumulation of HIF-1? in vitro and in vivo in colorectal carcinoma HCT116 cells under hypoxic conditions. Moreover, IDF-11774 treatment suppressed angiogenesis of cancer cells by reducing the expression of HIF-1 target genes, reduced glucose uptake, thereby sensitizing cells to growth under low glucose conditions, and decreased the extracellular acidification rate (ECAR) and oxygen consumption rate of cancer cells. Metabolic profiling of IDF-11774-treated cells revealed low levels of NAD(+), NADP(+), and lactate, as well as of intermediates in glycolysis and the tricarboxylic acid cycle. In addition, we observed elevated AMP and diminished ATP levels, resulting in a high AMP/ATP ratio. The level of AMP-activated protein kinase phosphorylation also increased, leading to inhibition of mTOR signaling in treated cells. In vivo xenograft assays demonstrated that IDF-11774 exhibited substantial anticancer efficacy in mouse models containing KRAS, PTEN, or VHL mutations, which often occur in malignant cancers. Collectively, our data indicate that IDF-11774 suppressed hypoxia-induced HIF-1? accumulation and repressed tumor growth by targeting energy production-related cancer metabolism. Twit Text FOAVip The novel hypoxia-inducible factor-1 inhibitor IDF-11774 regulates cancer metabolism, thereby suppressing tumor growth ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28569777 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28569777 #FOAvip English Wikipedia <ref>{{Cite pmid|28569777 }}</ref> The novel hypoxia-inducible factor-1? inhibitor IDF-11774 regulates cancer metabolism, thereby suppressing tumor growth #MMPMID28569777 Ban HS ; Kim BK ; Lee H ; Kim HM ; Harmalkar D ; Nam M ; Park SK ; Lee K ; Park JT ; Kim I ; Lee K ; Hwang GS ; Won M Cell Death Dis 2017[Jun]; 8 (6 ): e2843 PMID28569777 show ga HIF-1 is associated with poor prognoses and therapeutic resistance in cancer patients. We previously developed a novel hypoxia-inducible factor (HIF)-1 inhibitor, IDF-11774, a clinical candidate for cancer therapy. We also reported that IDF-1174 inhibited HSP70 chaperone activity and suppressed accumulation of HIF-1?. In this study, IDF-11774 inhibited the accumulation of HIF-1? in vitro and in vivo in colorectal carcinoma HCT116 cells under hypoxic conditions. Moreover, IDF-11774 treatment suppressed angiogenesis of cancer cells by reducing the expression of HIF-1 target genes, reduced glucose uptake, thereby sensitizing cells to growth under low glucose conditions, and decreased the extracellular acidification rate (ECAR) and oxygen consumption rate of cancer cells. Metabolic profiling of IDF-11774-treated cells revealed low levels of NAD(+), NADP(+), and lactate, as well as of intermediates in glycolysis and the tricarboxylic acid cycle. In addition, we observed elevated AMP and diminished ATP levels, resulting in a high AMP/ATP ratio. The level of AMP-activated protein kinase phosphorylation also increased, leading to inhibition of mTOR signaling in treated cells. In vivo xenograft assays demonstrated that IDF-11774 exhibited substantial anticancer efficacy in mouse models containing KRAS, PTEN, or VHL mutations, which often occur in malignant cancers. Collectively, our data indicate that IDF-11774 suppressed hypoxia-induced HIF-1? accumulation and repressed tumor growth by targeting energy production-related cancer metabolism. |*Gene Expression Regulation, Neoplastic [MESH] |Adamantane/*analogs & derivatives/pharmacology [MESH] |Animals [MESH] |Antineoplastic Agents/*pharmacology [MESH] |Cell Proliferation [MESH] |Colorectal Neoplasms/*drug therapy/genetics/metabolism/pathology [MESH] |Cyclic AMP/metabolism [MESH] |Female [MESH] |Glucose/metabolism [MESH] |Glycolysis/drug effects [MESH] |HCT116 Cells [MESH] |Humans [MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/*antagonists & inhibitors/genetics/metabolism [MESH] |Lactic Acid/metabolism [MESH] |Mice [MESH] |Mice, Nude [MESH] |NAD/metabolism [MESH] |Neovascularization, Pathologic/genetics/metabolism/pathology/*prevention & control [MESH] |PTEN Phosphohydrolase/genetics/metabolism [MESH] |Piperazines/*pharmacology [MESH] |Proto-Oncogene Proteins p21(ras)/genetics/metabolism [MESH] |Signal Transduction [MESH] |TOR Serine-Threonine Kinases/genetics/metabolism [MESH] |Von Hippel-Lindau Tumor Suppressor Protein/genetics/metabolism [MESH]The novel hypoxia-inducible factor-1? inhibitor IDF-11774 regulates ca(epmc).pdf DeepDyve Pubget Overpricing