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Analysis of AP-1 regulation on Smad3 genome-wide DNA binding sites in resistant basal cell carcinoma

ABSTRACT: Analysis of AP-1 regulation on Smad3 genome-wide DNA binding sites in resistant basal cell carcinoma

PROVIDER: PRJNA597071 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10751886.fastq.gz	Fastqsanger.gz
	SRR10751887.fastq.gz	Fastqsanger.gz
	SRR10751888.fastq.gz	Fastqsanger.gz
	SRR10751889.fastq.gz	Fastqsanger.gz
	SRR10751890.fastq.gz	Fastqsanger.gz

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Analysis of AP-1 regulation on Smad3 genome-wide DNA binding sites in resistant basal cell carcinoma

Project description:Tumor heterogeneity and lack of knowledge about resistant cell states remain a significant barrier to effective targeted cancer therapies. Basal cell carcinomas (BCCs) uniformly depend on Hedgehog (Hh)/Gli signaling for cell growth. We previously identified a nuclear myocardin-related transcription factor (nMRTF) resistance pathway that amplifies Gli1 activity, but nMRTF cell state and key factors driving its accumulation remain unknown. Epigenetic analysis of isolated nMRTF human tumor subpopulations demonstrates that cooperative AP-1 and TGFß signaling drive nMRTF activation. In this study, we find that AP-1 signaling drives changes in chromatin accessibility leading to differential Smad3 DNA binding and a transcriptional program of upstream activators of Rho, including RhoGEFs, that facilitate nMRTF activity.

2020-08-25 | GSE142469 | GEO

AP-1 dependent changes in chromatin accessibility in resistant basal cell carcinoma cell line

Project description:Tumor heterogeneity and lack of knowledge about resistant cell states remain a significant barrier to effective targeted cancer therapies. Basal cell carcinomas (BCCs) uniformly depend on Hedgehog (Hh)/Gli signaling for cell growth. We previously identified a nuclear myocardin-related transcription factor (nMRTF) resistance pathway that amplifies Gli1 activity, but nMRTF cell state and key factors driving its accumulation remain unknown. We have determined that AP-1 transcription factor activity is essential to maintain MRTF activation. Here, we treat a murine BCC cell line with small molecule AP-1 inhibitor and analyze chromatin accessibility profiles.

2020-08-25 | GSE156764 | GEO

AP-1 and TGFb-dependent transcriptomic changes in resistant basal cell carcinoma cell line

Project description:Tumor heterogeneity and lack of knowledge about resistant cell states remain a significant barrier to effective targeted cancer therapies. Basal cell carcinomas (BCCs) uniformly depend on Hedgehog (Hh)/Gli signaling for cell growth. We previously identified a nuclear myocardin-related transcription factor (nMRTF) resistance pathway that amplifies Gli1 activity, but nMRTF cell state and key factors driving its accumulation remain unknown. We have determined that AP-1 and TGFb transcription factor activity is essential to maintain MRTF activation. Here, we treat a murine BCC cell line with small molecule AP-1 and ALK5 inhibitors and analyze transcriptomic profiles.

2020-08-25 | GSE156789 | GEO

Genome-wide maps of apurinic sites (AP-sites) and 8-oxoG derived secondary AP-sites

Project description:Genome-wide maps of apurinic sites (AP-sites) and 8-oxoG derived secondary AP-sites

| PRJNA497112 | ENA

Genome-wide maps of apurinic sites (AP-sites) and 8-oxoG derived secondary AP-sites

Project description:We developed a novel method, AP-seq, capable of mapping apurinic sites and 8-oxo-7,8-dihydroguanine bases at approximately 250bp resolution on a genome-wide scale. We directly demonstrate that the accumulation rate of apurinic sites varies widely across the genome, with hot spots acquiring many times more damage than cold spots. The experiment was performed in triplicates on HepG2 cells, 30 min after X-ray treatment (6Gy). AP-Seq is an approach that specifically enriches AP-sites via a biotin-labelled aldehyde-reactive probe under pH neutral conditions, which has been well established for the specific detection of AP-sites since its development by Kubo et al. in 1992. Under neutral conditions (pH7), 1h at 37ºC, the probe is highly specific for the aldehydes occurring at AP-sites. After biotin labelling of genomic DNA, DNA is sonicated into ~250 bp fragments, enriched, in vitro repaired (PreCR, NEB), and used for Illumina short read sequencing (125 bp, paired end, HiSeq2000). To assess oxidative damage as the sum of AP-sites and 8-oxoG, we applied recombinant OGG1 in vitro to the extracted DNA (OGG1-AP-seq). Under the conditions chosen, any remaining 8-oxoG is excised in a largely sequence-independent fashion after DNA extraction to result in a set of secondary AP-sites and to a lesser extent the associated beta-elimination product.

2018-10-22 | GSE121005 | GEO

Smad3, Smad4 and TTF-1/NKX2-1 binding sites in H441/A549 lung cancer cell lines

Project description:We evaluated the role of TTF-1/NKX2-1 on Smad3 and Smad4 binding in lung cancer cell lines. Smad3 binding sites in A549 cells and Smad3, Smad4, and TTF-1/NKX2-1 binding sites in H441 cells were determined by ChIP-seq.

2014-07-27 | E-GEOD-51509 | biostudies-arrayexpress

Smad2 and Smad3 binding sites in H345-TbRII cells

Project description:Transforming growth factor (TGF)-beta induces apoptosis of many types of cancer cells and acts as a tumor suppressor. We found lower expression of TGF-beta type II receptor (TbRII) in most of SCLC cells and tissues than in normal lung epithelial cells and normal lung tissues, respectively. In vitro cell growth and in vivo tumor formation were suppressed by TGF-beta-mediated apoptosis when the wild-type TbRII was overexpressed in SCLC cells. We therefore determined Smad2 and Smad3 (Smad2/3) binding sites in a SCLC cell line H345 stably expressing exogenous TbRII (H345-TbRII) to identify target genes of TGF-beta. Smad2 and Smad3 binding sites in H345-TbRII cells were determined by ChIP-seq (one sample analysis, without replicates).

2015-09-15 | E-GEOD-63871 | biostudies-arrayexpress

AP-1 and TGFb-dependent transcriptomic changes in resistant basal cell carcinoma cell line

Project description:AP-1 and TGFb-dependent transcriptomic changes in resistant basal cell carcinoma cell line

| PRJNA659018 | ENA

AP-1 dependent changes in chromatin accessibility in resistant basal cell carcinoma cell line

Project description:AP-1 dependent changes in chromatin accessibility in resistant basal cell carcinoma cell line

| PRJNA658994 | ENA

AP-1 and TGFb cooperativity drives non-canonical Hedgehog signaling in resistant basal cell carcinoma

Project description:AP-1 and TGFb cooperativity drives non-canonical Hedgehog signaling in resistant basal cell carcinoma

| PRJNA659351 | ENA