HIF‐1α induces cell cycle arrest by functionally counteracting Myc

By M. Koshiji, Y. Kageyama, Erin A Pete, I. Horikawa, J. Barrett, L. E. Huang. 2004

608 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/3dfbd74785ad867d8c834fe6766f463a422ec970

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. G. Semenza
2. M. C. Simon
3. P. Ratcliffe
4. Craig B. Thompson
5. Adrian L. Harris
6. C. V. Dang
7. S. Påhlman
8. C. Wigerup

In Molecular Biology

1. G. Semenza
2. M. C. Simon
3. P. Ratcliffe
4. Adrian L. Harris
5. Craig B. Thompson
6. S. Påhlman
7. C. Wigerup
8. D. Bexell

In Oncology

1. V. Plaks
2. G. Semenza
3. Zena Werb
4. M. C. Simon
5. Adrian L. Harris
6. Craig B. Thompson
7. Niwen Kong
8. Pengfei Lu

Citations in the corpus

• Lost in transcription: p21 repression, mechanisms, and consequences. (2005, background): “In a similar manner, hypoxia inducible factor 1a displaces c-Myc from the p21 promoter leading to transcriptional activation of p21 and subsequent growth arrest (34).”
• Therapeutic targeting of hypoxia and hypoxia-inducible factors in cancer. (2016, background): “Intriguingly, HIF-1 and HIF-2 often have opposing effects on tumor growth, for instance on crucial cell cycle and apoptotic regulators like c-MYCandp53.”
• HIF-2alpha promotes hypoxic cell proliferation by enhancing c-myc transcriptional activity. (2007, methodology): “We confirmed published data concerning HIF-a subunit expression and localization in these cells (Koshiji et al., 2004; Maxwell et al., 1999).”
• Oxygen in stem cell biology: a critical component of the stem cell niche. (2010, background): “HIF-1 has emerged as a likely candidate of this regulatory mechanism, as several groups have demonstrated that HIF can mediate cell-cycle arrest in several cell lines (Koshiji et al., 2004).”
• Integration of Oxygen Signaling at the Consensus HRE (2005, neutral): “STAT3 (target gene–specific) (116) C/EBPα (target gene–specific) (117) Ets-1 (target gene–specific; Flk-1; HIF-2α–specific) (59) Myc (counteracted by HIF-1α) (118) p14ARF (nucleolar sequestration) (119)”
• Contrasting Properties of Hypoxia-Inducible Factor 1 (HIF-1) and HIF-2 in von Hippel-Lindau-Associated Renal Cell Carcinoma (2005, background): “Interestingly, HIF-1 has recently been demonstrated to antagonize Myc and induce cell cycle arrest by complexing Myc in a transcriptionally inactive form ( 20 ).”
• ADAPTIVE AND MALADAPTIVE CARDIORESPIRATORY RESPONSES TO CONTINUOUS AND INTERMITTENT HYPOXIA MEDIATED BY HYPOXIA-INDUCIBLE FACTORS 1 AND 2 (2012, background): “There are now several examples in which HIF-1 binds to other transcription factors and blocks the assembly of transactivation complexes (164, 165).”
• HIF and c-Myc: sibling rivals for control of cancer cell metabolism and proliferation. (2007, background): “Surprisingly, this occurs not only at the c-Myc repressed target p21 (Koshiji et al., 2004), where Sp1 is required, but also at c-Myc activated targets MSH2, MSH6, and Nbs1 (Koshiji et al., 2005; To et al., 2006).”
• Direct regulation of TWIST by HIF-1α promotes metastasis (2008, neutral): “Transfection with an inactive HIF-1α mutant (HIF-1α(LCLL)”
• The Cancer Stem Cell Niche: How Essential is the Niche in Regulating Stemness of Tumor Cells? (2015, positive): “HIF-1a antagonizes Myelocytomatosis viral oncogene homolog (c-Myc) activation, thus slowing down cell-cycle progression to protect CSCs from DNA damage and enhance stemness (Koshiji et al., 2004).”