ArticleCell reports2015
Deregulation of the Ras-Erk Signaling Axis Modulates the Enhancer Landscape.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
- Enhancer Remodeling during Adaptive Bypass to MEK Inhibition Is Attenuated by Pharmacologic Targeting of the P-TEFb Complex.Cancer discovery · 2017Trial
- RIPOR2 promotes multinucleation of melanoma cells downstream of the RAS/ERK oncogenic pathway.iScience · 2026Article
- Cell-context response to germ layer differentiation signals is predetermined by the epigenome in regionalized epiblast populations.Nature communications · 2025Article
- Current progress and future perspective of super-enhancers: a viable and effective bridge between the transcriptional apparatus and disease.Frontiers in genetics · 2025Review
- Integration of single-cell transcriptomics and epigenetic analysis reveals enhancer-controlled TIMP1 as a regulator of ferroptosis in colorectal cancer.Genes & genomics · 2024Article
- AP-1 signaling pathway promotes pro-IL-1β transcription to facilitate NLRP3 inflammasome activation upon influenza A virus infection.Virulence · 2022Article
- An oncogenic enhancer encodes selective selenium dependency in AML.Cell stem cell · 2022Article
- Article
- Epigenetic Regulation of Inflammatory Signaling and Inflammation-Induced Cancer.Frontiers in cell and developmental biology · 2022Review
- Master lineage transcription factors anchor trans mega transcriptional complexes at highly accessible enhancer sites to promote long-range chromatin clustering and transcription of distal target genes.Nucleic acids research · 2021Article
- Review
- Targeting transcriptional regulators for treatment of anaplastic thyroid cancer.Journal of cancer metastasis and treatment · 2021Article
- Dynamic Interactions of Transcription Factors and Enhancer Reprogramming in Cancer Progression.Frontiers in oncology · 2021Review
- Genomic retargeting of p53 and CTCF is associated with transcriptional changes during oncogenic HRas-induced transformation.Communications biology · 2020Article
- Illuminating the noncoding genome in cancer.Nature cancer · 2020Review
- Oncogenic super-enhancer formation in tumorigenesis and its molecular mechanisms.Experimental & molecular medicine · 2020Review
- Enhancer Domains in Gastrointestinal Stromal Tumor Regulate KIT Expression and Are Targetable by BET Bromodomain Inhibition.Cancer research · 2019Article
- Chromatin regulator Asxl1 loss and Nf1 haploinsufficiency cooperate to accelerate myeloid malignancy.The Journal of clinical investigation · 2018Article
- Hypermethylation of gene body CpG islands predicts high dosage of functional oncogenes in liver cancer.Nature communications · 2018Article
- MEK inhibition induces MYOG and remodels super-enhancers in RAS-driven rhabdomyosarcoma.Science translational medicine · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Unrestrained receptor tyrosine kinase (RTK) signaling and epigenetic deregulation are root causes of tumorigenesis. We establish linkage between these processes by demonstrating that aberrant RTK signaling unleashed by oncogenic HRas(G12V) or loss of negative feedback through Sprouty gene deletion remodels histone modifications associated with active typical and super-enhancers. However, although both lesions disrupt the Ras-Erk axis, the expression programs, enhancer signatures, and transcription factor networks modulated upon HRas(G12V) transformation or Sprouty deletion are largely distinct. Oncogenic HRas(G12V) elevates histone 3 lysine 27 acetylation (H3K27ac) levels at enhancers near the transcription factor Gata4 and the kinase Prkcb, as well as their expression levels. We show that Gata4 is necessary for the aberrant gene expression and H3K27ac marking at enhancers, and Prkcb is required for the oncogenic effects of HRas(G12V)-driven cells. Taken together, our findings demonstrate that dynamic reprogramming of the cellular enhancer landscape is a major effect of oncogenic RTK signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.