
NCBI . NLM . NIH . GOV {
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Title[redir]:
HIF and c-Myc: sibling rivals for control of cancer cell metabolism and proliferation - PMC
Description:
O2 deprivation (hypoxia) and cellular proliferation engage opposite cellular pathways, yet often coexist during tumor growth. The ability of cells to grow during hypoxia results in part from crosstalk between hypoxia inducible factors (HIFs) and the ...
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Keywords {🔍}
doi, cmyc, cell, pubmed, google, scholar, hifα, hif, expression, pmc, growth, article, mitochondrial, free, hypoxia, effects, cancer, tumor, targets, complex, cells, metabolism, translation, transcriptional, proliferation, factor, transcription, synthesis, mxi, biol, protein, activity, genes, tumors, gene, pathways, cycle, levels, pyruvate, hifalpha, carbon, target, simon, glycolytic, promotes, activation, dang, mol, nlm, cellular,
Topics {✒️}
altered c-myc/max stoichiometry increasing c-myc/max interactions c-myc activated target c-myc potently enhances c-myc promotes ribosome c-myc mediated lymphomagenesis c-myc transcriptional activity c-myc driven proliferation adipose differentiation-related protein pmc beta search pol iii-dependent expression c-myc null fibroblasts disrupt c-myc complexes c-myc target genes stable β-subunit arnt pol i-dependent expression enhancing c-myc function hypoxia-inducible factor 1alpha c-myc activated targets triggers eif-2α phosphorylation c-myc/hifs interactions c-myc transcriptional targets c-myc/max association characterized hif-α subunits c-myc repressed targets vhl-deficient renal tumors hypoxia-inducible factor-1 targeting increased c-myc effects hif-2alpha regulates oct-4 growth factor-dependent regulation oncogene-induced genetic instability limiting c-myc influences c-myc promoted processes c-myc-induced apoptosis shed glucose-derived carbon chronic hif-α stabilization hypoxia-induced paralogs scylla triglyceride-loaded foam cells hif-2α/arnt targets hif-1α/arnt dimers hif-2α occur rapidly direct hif-α effects proto-oncogene c-myc reinforce hif-1α effects additional hif-independent effect c-myc targets odc mtorc1 phosphorylates 4e-bp c-myc induced transformation hif-1α binds directly cell cycle arrest
Questions {❓}
- How do cancer cells acquire the fuel needed to support cell growth?
- Why does c-Myc promote both mitochondrial biogenesis and a metabolic shift towards glycolysis?
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