U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination

SRX4672370: GSM3385023: A549_HIF1bChIPseq_r2; Homo sapiens; ChIP-Seq
1 ILLUMINA (Illumina HiSeq 2500) run: 20.2M spots, 1G bases, 454.1Mb downloads

Submitted by: NCBI (GEO)
Study: DNA methylation repels binding of hypoxia-inducible transcription factors to maintain tumour immunotolerance [ChIPSeq]
show Abstracthide Abstract
Background: Hypoxia is pervasive in cancer and other diseases. Cells sense and adapt to hypoxia by activating hypoxia-inducible transcription factors (HIFs), but it is still an outstanding question why cell types differ in their transcriptional response to hypoxia. Results: Here, we report that HIFs fail to bind CpG dinucleotides that are methylated in their consensus binding sequence, both in in vitro biochemical binding assays and in vivo studies of differentially methylated isogenic cell lines. Based on in silico structural modelling, we show that 5-methylcytosine indeed causes steric hindrance in the HIF binding pocket. A model wherein cell-type-specific methylation landscapes, as laid-down by the differential expression and binding of other transcription factors under normoxia control cell-type-specific hypoxia responses is observed. We also discover ectopic HIF binding sites in repeat regions which are normally methylated. Genetic and pharmacological DNA demethylation, but also cancer-associated DNA hypomethylation, expose these binding sites, inducing HIF-dependent expression of cryptic transcripts. In line with such cryptic transcripts being more prone to cause double-stranded RNA and viral mimicry, we observe low DNA methylation and high cryptic transcript expression in tumours with high immune checkpoint expression, but not in tumours with low immune checkpoint expression, where they would compromise tumour immunotolerance. In a low-immunogenic tumour model, DNA demethylation upregulates cryptic transcript expression in a HIF-dependent manner, causing immune activation and reducing tumour growth. Conclusions: Our data elucidate the mechanism underlying cell-type specific responses to hypoxia, and suggest DNA methylation and hypoxia to underlie tumour immunotolerance. Overall design: Examination of genome wide HIF1b binding sites in 4 human cancer cell lines, one demethylated cancer cell line and mouse ES Dnmt-WT and Dnmt-TKO cell lines by HIF1b ChIP-seq
Sample: A549_HIF1bChIPseq_r2
SAMN10037529 • SRS3767075 • All experiments • All runs
Organism: Homo sapiens
Library:
Instrument: Illumina HiSeq 2500
Strategy: ChIP-Seq
Source: GENOMIC
Selection: ChIP
Layout: SINGLE
Construction protocol: Cells were incubated in hypoxic conditions for 16 hours. Cultured cells were subsequently immediately fixed by adding 1% Formaldehyde (16% Formaldehyde (w/v), Methanol-free, Thermo Scientific) directly in the medium and incubating for 8 minutes. Fixed cells were incubated with 150 mM of glycine for 5 min to revert the cross-links, washed twice with ice-cold PBS 0.5% Triton-X100, scraped and collected by centrifugation (1000 ×G 5min at 4°C). The pellet was resuspended in 1400 µL of RIPA buffer (50 mM Tris-HCl pH 8, 150 mM NaCl, 2 mM EDTA pH 8, 1% Triton-X100, 0.5% Sodium deoxycholate, 1% SDS, 1% protease inhibitors) and transferred in a new eppendorf tube. The chromatin was sonicated for 3 min by using a Branson 250 Digital Sonifier with 0.7 s 'On' and 1.3 s 'Off' pulses at 40% power amplitude, yielding a size of 100 to 500 bp. The sample was kept ice-cold at all times during the sonication. The samples were centrifuged (10 min at 16000 ×G at 4°C) and the supernatant were transferred in a new eppendorf tube. The protein concentration was assessed using a BCA assay. Fifty µL of shared chromatin was used as “input” and 1.4 µg of primary ARNT/HIF-1β monoclonal antibody (NB100-124, Novus) per 1 mg of protein was added to the remainder of the chromatin, and incubated overnight at 4°C in a rotator. Pierce Protein A/G Magnetic Beads (Life Technologies) were added to the samples in a volume that is 4X the volume of the primary Ab and incubated at 4°C for at least 5 hours. A/G Magnetic Beads were collected and the samples were washed 5 times with the washing buffer (50 mM Tris-HCl, 200 mM LiCl, 2 mM EDTA, pH 8, 1% Triton, 0.5% Sodium deoxycholate, 0.1% SDS, 1% protease inhibitors), and twice with TE buffer. The A/G magnetic beads were resuspended in 50 µL of TE buffer, and 1.5 µL of RNAse A (200 units, NEB, Ipswich, MA, USA) were added to the A/G beads samples and to the input, incubated for 10 minutes at 37°C. After addition of 1.5 µL of proteinase K (200 units) and overnight incubation at 65°C, the DNA was purified using 1.8´ volume of Agencourt AMPure XP (Beckman Coulter) according to the manufactory instructions One µg of input and all of the immunoprecipitated DNA were converted into sequencing libraries using the NEBNext Ultra DNA library prep kit.
Experiment attributes:
GEO Accession: GSM3385023
Links:
Runs: 1 run, 20.2M spots, 1G bases, 454.1Mb
Run# of Spots# of BasesSizePublished
SRR782120320,245,6871G454.1Mb2020-06-18

ID:
6330819

Supplemental Content

Search details

See more...

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...