High-resolution genome-wide mapping of HIF-binding sites by ChIP-seq

Schödel, Johannes; Oikonomopoulos, Spyros; Ragoussis, Jiannis; Pugh, Christopher W.; Ratcliffe, Peter J.; Mole, David R.

doi:10.1182/blood-2010-10-314427

Cited by 619 publications

(703 citation statements)

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“…Although recent genome-wide analysis of SRC-3 chromatin affinity sites in MCF-7 human breast cancer in response to estrogen induction did not identify the MIF gene, high-stringency HIF-binding site(s) near the MIF gene was identified in another recent genome-wide mapping [42,66]. It is reasonable that as a master transcriptional regulator, the ability of SRC-3 to regulate expression of its target genes is dependent on the transcriptional factors involved (i.e., HIF-1 vs ERα).…”

Section: Discussionmentioning

confidence: 97%

“…Recently, genome-wide mapping has identified potential high-stringency hypoxia-inducible factor (HIF)-binding site(s) near the MIF gene [42]. Accordingly, the HIF-1alpha (HIF-1α) transcriptional factor has been reported to induce MIF expression by binding to the HRE of the MIF promoter [18,43].…”

Section: Phosphorylation Of S857 Is Required For the Coactivation Ofmentioning

confidence: 99%

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Steroid receptor coactivator 3 regulates autophagy in breast cancer cells through macrophage migration inhibitory factor

et al. 2012

Cell Res

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SRC-3/AIB1 (steroid receptor coactivator 3/amplified in breast cancer 1) is an authentic oncogene that contributes to the development of drug resistance and poor disease-free survival in cancer patients. Autophagy is also an important cell death mechanism that has tumor suppressor function. In this study, we identified macrophage migration inhibitory factor (MIF) as a novel target gene of SRC-3 and demonstrated its importance in cell survival. Specifically, we showed that MIF is a strong suppressor of autophagic cell death. We further showed that suppression of MIF, in turn, induced autophagic cell death, enhanced chemosensitivity and inhibited tumorigenesis in a xenograft mouse tumorigenesis model. Our study demonstrated that regulation of MIF expression and suppression of autophagic cell death is a potent mechanism by which SRC-3 contributes to increased chemoresistance and tumorigenicity.

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Section: Discussionmentioning

confidence: 97%

Section: Phosphorylation Of S857 Is Required For the Coactivation Ofmentioning

confidence: 99%

Steroid receptor coactivator 3 regulates autophagy in breast cancer cells through macrophage migration inhibitory factor

et al. 2012

Cell Res

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“…22 However, PTK6 has not previously been identified as a HIF target, since no HIF binding to PTK6 promoter was identified in larger genome-wide ChIP-seq studies. 23,24 This indicated that there might be other parallel mechanisms for hypoxia-mediated PTK6 induction.…”

Section: Ptk6 (Protein Tyrosinementioning

confidence: 96%

HIF-1α-independent hypoxia-induced rapid PTK6 stabilization is associated with increased motility and invasion

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Broos

et al. 2014

Cancer Biology & Therapy

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“…For example, binding of CREB 51 and GADD45B 52 in the BDNF region upstream of the rs6265 SNP has been detected. Moreover, BHLHB2 and GADD45B are regulated by hypoxia, since they have a highstringency HIF1 binding site, 53,54 and BHLHB2 represses expression of MITF, 53 a TF stimulating HIF1a expression. 55 Studies in mice have also proved how the basic helix-loop-helix protein BHLHB2 is regulated by neurotrophins and modulate BDNF transcription.…”

Section: Relationship Between Rs6265 Genotype and Dna-protein Bindingmentioning

confidence: 99%

BDNF rs6265 methylation and genotype interact on risk for schizophrenia

et al. 2016

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Epigenetic mechanisms can mediate gene-environment interactions relevant for complex disorders. The BDNF gene is crucial for development and brain plasticity, is sensitive to environmental stressors, such as hypoxia, and harbors the functional SNP rs6265 (Val 66 Met), which creates or abolishes a CpG dinucleotide for DNA methylation. We found that methylation at the BDNF rs6265 Val allele in peripheral blood of healthy subjects is associated with hypoxia-related early life events (hOCs) and intermediate phenotypes for schizophrenia in a distinctive manner, depending on rs6265 genotype: in ValVal individuals increased methylation is associated with exposure to hOCs and impaired working memory (WM) accuracy, while the opposite is true for ValMet subjects. Also, rs6265 methylation and hOCs interact in modulating WM-related prefrontal activity, another intermediate phenotype for schizophrenia, with an analogous opposite direction in the 2 genotypes. Consistently, rs6265 methylation has a different association with schizophrenia risk in ValVals and ValMets. The relationships of methylation with BDNF levels and of genotype with BHLHB2 binding likely contribute to these opposite effects of methylation. We conclude that BDNF rs6265 methylation interacts with genotype to bridge early environmental exposures to adult phenotypes, relevant for schizophrenia. The study of epigenetic changes in regions containing genetic variation relevant for human diseases may have beneficial implications for the understanding of how genes are actually translated into phenotypes.

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High-resolution genome-wide mapping of HIF-binding sites by ChIP-seq

Cited by 619 publications

References 50 publications

Steroid receptor coactivator 3 regulates autophagy in breast cancer cells through macrophage migration inhibitory factor

Steroid receptor coactivator 3 regulates autophagy in breast cancer cells through macrophage migration inhibitory factor

HIF-1α-independent hypoxia-induced rapid PTK6 stabilization is associated with increased motility and invasion

BDNF rs6265 methylation and genotype interact on risk for schizophrenia

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