ArticleEpigenetics & chromatin2015
STAT3 acts through pre-existing nucleosome-depleted regions bound by FOS during an epigenetic switch linking inflammation to cancer.
Article in Epigenetics & chromatin, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- IL-10's contextual role in cytotoxic antitumor immunity: evidence, controversies, and therapeutic translation.Frontiers in immunology · 2026Review
- Endothelial cells retain inflammatory memory through chromatin remodeling in a two-hit model of infection-induced inflammation.American journal of physiology. Cell physiology · 2025Article
- Review
- MafB, WDR77, and ß-catenin interact with each other and have similar genome association profiles.PloS one · 2022Article
- Different SP1 binding dynamics at individual genomic loci in human cells.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Article
- S100A8/S100A9 cytokine acts as a transcriptional coactivator during breast cellular transformation.Science advances · 2021Article
- Stable intronic sequence RNAs (sisRNAs) are selected regions in introns with distinct properties.BMC genomics · 2020Article
- Fine-mapping of a novel premenopausal breast cancer susceptibility locus at Chr4q31.22 in Caucasian women and validation in African and Chinese women.International journal of cancer · 2020Observational
- BCL9/STAT3 regulation of transcriptional enhancer networks promote DCIS progression.NPJ breast cancer · 2020Article
- Article
- Review
- Satb1 integrates DNA binding site geometry and torsional stress to differentially target nucleosome-dense regions.Nature communications · 2019Article
- Inflammatory regulatory network mediated by the joint action of NF-kB, STAT3, and AP-1 factors is involved in many human cancers.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- IL1-Induced JAK/STAT Signaling Is Antagonized by TGFβ to Shape CAF Heterogeneity in Pancreatic Ductal Adenocarcinoma.Cancer discovery · 2019Article
- The ASD Living Biology: from cell proliferation to clinical phenotype.Molecular psychiatry · 2019Review
- Risk Locus Identification Ties Alcohol Withdrawal Symptoms to SORCS2.Alcoholism, clinical and experimental research · 2018Article
- Genome-scale identification of transcription factors that mediate an inflammatory network during breast cellular transformation.Nature communications · 2018Article
- Heterochromatin Reduction Correlates with the Increase of the KDM4B and KDM6A Demethylases and the Expression of Pericentromeric DNA during the Acquisition of a Transformed Phenotype.Journal of Cancer · 2017Article
- LINC00520 is induced by Src, STAT3, and PI3K and plays a functional role in breast cancer.Oncotarget · 2016Article
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
backgroundTransient induction of the Src oncoprotein in a non-transformed breast cell line can initiate an epigenetic switch to a cancer cell via a positive feedback loop that involves activation of the signal transducer and activator of transcription 3 protein (STAT3) and NF-κB transcription factors.
resultsWe show that during the transformation process, nucleosome-depleted regions (defined by formaldehyde-assisted isolation of regulatory elements (FAIRE)) are largely unchanged and that both before and during transformation, STAT3 binds almost exclusively to previously open chromatin regions. Roughly, a third of the transformation-inducible genes require STAT3 for the induction. STAT3 and NF-κB appear to drive the regulation of different gene sets during the transformation process. Interestingly, STAT3 directly regulates the expression of NFKB1, which encodes a subunit of NF-κB, and IL6, a cytokine that stimulates STAT3 activity. Lastly, many STAT3 binding sites are also bound by FOS and the expression of several AP-1 factors is altered during transformation in a STAT3-dependent manner, suggesting that STAT3 may cooperate with AP-1 proteins.
conclusionsThese observations uncover additional complexities to the inflammatory feedback loop that are likely to contribute to the epigenetic switch. In addition, gene expression changes during transformation, whether driven by pre-existing or induced transcription factors, occur largely through pre-existing nucleosome-depleted regions.
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