Journal article icon

Journal article

Genetic variation at the 8q24.21 renal cancer susceptibility locus affects HIF binding to a MYC enhancer

Abstract:
Clear cell renal cell carcinoma (ccRCC) is characterized by loss of function of the von Hippel-Lindau tumour suppressor (VHL) and unrestrained activation of hypoxia-inducible transcription factors (HIFs). Genetic and epigenetic determinants have an impact on HIF pathways. A recent genome-wide association study on renal cancer susceptibility identified single-nucleotide polymorphisms (SNPs) in an intergenic region located between the oncogenes MYC and PVT1. Here using assays of chromatin conformation, allele-specific chromatin immunoprecipitation and genome editing, we show that HIF binding to this regulatory element is necessary to trans-activate MYC and PVT1 expression specifically in cells of renal tubular origins. Moreover, we demonstrate that the risk-associated polymorphisms increase chromatin accessibility and activity as well as HIF binding to the enhancer. These findings provide further evidence that genetic variation at HIF-binding sites modulates the oncogenic transcriptional output of the VHL-HIF axis and provide a functional explanation for the disease-associated effects of SNPs in ccRCC.
Publication status:
Published
Peer review status:
Peer reviewed

Actions


Access Document


Files:
Publisher copy:
10.1038/ncomms13183

Authors


More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Role:
Author



Publisher:
Nature Publishing Group
Journal:
Nature Communications More from this journal
Volume:
7
Pages:
13183
Publication date:
2016-10-24
Acceptance date:
2016-09-08
DOI:
EISSN:
2041-1723


Language:
English
Keywords:
Pubs id:
pubs:655091
UUID:
uuid:a1c166e7-07a8-4a26-8eb8-0e65500dcd8c
Local pid:
pubs:655091
Source identifiers:
655091
Deposit date:
2016-11-02

Terms of use



Views and Downloads






If you are the owner of this record, you can report an update to it here: Report update to this record

TO TOP