PubMed:23999440 JSONTXT

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{"project":"DisGeNet-2017-sample","denotations":[{"id":"T2921","span":{"begin":525,"end":530},"obj":"gene:3091"},{"id":"T2922","span":{"begin":726,"end":744},"obj":"disease:C0178874"},{"id":"T2923","span":{"begin":656,"end":660},"obj":"gene:5290"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T2921","obj":"T2922"},{"id":"R2","pred":"associated_with","subj":"T2921","obj":"T2922"},{"id":"R3","pred":"associated_with","subj":"T2923","obj":"T2922"},{"id":"R4","pred":"associated_with","subj":"T2923","obj":"T2922"},{"id":"R5","pred":"associated_with","subj":"T2923","obj":"T2922"},{"id":"R6","pred":"associated_with","subj":"T2923","obj":"T2922"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"HIF-1 mediates metabolic responses to intratumoral hypoxia and oncogenic mutations.\nHypoxia occurs frequently in human cancers and induces adaptive changes in cell metabolism that include a switch from oxidative phosphorylation to glycolysis, increased glycogen synthesis, and a switch from glucose to glutamine as the major substrate for fatty acid synthesis. This broad metabolic reprogramming is coordinated at the transcriptional level by HIF-1, which functions as a master regulator to balance oxygen supply and demand. HIF-1 is also activated in cancer cells by tumor suppressor (e.g., VHL) loss of function and oncogene gain of function (leading to PI3K/AKT/mTOR activity) and mediates metabolic alterations that drive cancer progression and resistance to therapy. Inhibitors of HIF-1 or metabolic enzymes may impair the metabolic flexibility of cancer cells and make them more sensitive to anticancer drugs."}