HIF and c-Myc: sibling rivals for control of cancer cell metabolism and proliferation.

By John D. Gordan, Craig B. Thompson, M. C. Simon. Cancer Cell, 2007

826 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/f35f28f8bc4031d44bf71ae8bc572f0c78f85fd6

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. C. V. Dang
2. G. Semenza
3. David M. Sabatini
4. Erika L. Pearce
5. M. V. Vander Heiden
6. Ping Gao
7. J. Pouysségur
8. J. Cantor

In Molecular Biology

1. C. V. Dang
2. David M. Sabatini
3. G. Semenza
4. M. V. Vander Heiden
5. Ping Gao
6. J. Cantor
7. Alexey I. Nesvizhskii
8. B. Manning

In Oncology

1. M. Gubin
2. David M. Sabatini
3. D. Sinclair
4. Ping Gao
5. C. V. Dang
6. M. C. Simon
7. Adrian L. Harris
8. Jung-whan Kim

Citations in the corpus

• Metabolic competition in the tumor microenvironment is a driver of cancer progression (2015, methodology): “Using a genetic gain-of-function approach, we transduced R tumors with retrovirus expressing c-Myc, a transcription factor that drives glycolysis (Gordan et al., 2007). c-Myc expressing R tumors (R-cMyc) displayed enhanced ECAR in vitro (Figure 3E), compared to R tumors expressing the empty vector…”
• An Integrated Metabolic Atlas of Clear Cell Renal Cell Carcinoma (2016, neutral): “One of the key HIF1 targets in glycolysis is pyruvate dehydrogenase kinase, which phosphorylates and inhibits pyruvate dehydrogenase (PDH), thereby impeding fueling of pyruvate-derived carbons to the TCA cycle (Gordan et al., 2007; Kaelin, 2008; Semenza, 2013).”
• Cancer cell metabolism: Warburg and beyond. (2008, background): “…downstream effector of insulin signaling, reprises its role in glucose uptake and utilization in the cancer setting (reviewed in Manning and Cantley, 2007), whereas the Myc transcription factor upregulates the expression of various metabolic genes (reviewed in Gordan et al., 2007).”
• Integrated Proteogenomic Characterization of Clear Cell Renal Cell Carcinoma (2019, background): “, 2007a, 2008), with MYC regulation of metabolism functioning in concert with and independent of HIF-1 signaling (Gordan et al., 2007b).”
• Activation of a metabolic gene regulatory network downstream of mTOR complex 1. (2010, background): “Importantly, the transcription factor hypoxiainducible factor (HIF1) stimulates the same genes of glycolysis and, like c-Myc, is a basic helix loop helix (bHLH) transcription factor that recognizes an overlapping promoterbinding element (Table 1; Gordan et al., 2007; Semenza, 2003).”
• c-Myc and Cancer Metabolism (2012, neutral): “48) andhas been shown to upregulate expression of a broad variety of metabolic enzymes (49).”
• Hypoxia and cancer (2007, background): “Gene-profile selectivity may also arise from differential action of the three HIF-α subunits and, within the context, may promote cell proliferation or death [21, 22].”
• Acetylation Targets the M2 Isoform of Pyruvate Kinase for Degradation through Chaperone-Mediated Autophagy and Promotes Tumor Growth (2011, neutral): “…of oncogenes or loss of tumor suppressor genes, such as mutations in Ras (Dang and Semenza, 1999; Ramanathan et al., 2005), AKT (Manning and Cantley, 2007), Myc (Gordan et al., 2007a, 2007b), and p53 (Bensaad et al., 2006; Matoba et al., 2006) increase glucose uptake and lactate production.”
• Hypoxia-induced angiogenesis: good and evil. (2011, background): “Alternatively, HIF-2α may contribute to the ischemic phenotypes in Phd1 skeletal muscle by regulating redox homeostasis.(151,152) These studies demonstrate the diverse mechanisms through which hypoxia and the HIF pathway regulate vascular responses to tissue hypoxia and ischemia.”
• The interplay between MYC and HIF in cancer (2008, background): “The hypoxia-inducible factors, HIF1 and HIF2 (also known as EPAS1 ), provide transcriptional homeostatic responses to limited oxygen levels that are prevalent in both physiological and pathological condition”
• Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging (2013, background): “In cancer cells, metabolic reprogramming is mediated by crosstalk between HIF-1a and c-Myc (Gordan et al., 2007), raising the possibility that c-Myc was the missing factor.”
• Fatty acid uptake and lipid storage induced by HIF-1α contribute to cell growth and survival after hypoxia-reoxygenation. (2014, background): “Many genes that are already known to be HIF-1a targets were induced, including genes involved in metabolic processes (Gordan et al., 2007; Stubbs and Griffiths, 2010).”
• Reprogramming of human primary somatic cells by OCT4 and chemical compounds. (2010, background): “…hypoxic conditions/ HIF-1a, and the reprogramming factor Cell Stem Cell 7, MYC all regulate various aspects of cellular metabolism, including the upregulation of glucose transporters and metabolic enzymes of glycolysis, such as GLUT1, HK2, and PFK1 (Gordan et al., 2007; DeBerardinis et al., 2008).”
• The impact of O2 availability on human cancer (2008, background): “These observations describe crosstalk between responses to changes in O 2 availability and a key transcription factor regulating cell growt”