ArticleOncogenesis2020
Aberrant super-enhancer landscape reveals core transcriptional regulatory circuitry in lung adenocarcinoma.
Article in Oncogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The trial behind it
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Who cites it
29 citing papers in PubMed.
- A core transcriptional regulatory circuitry controls super-enhancer-driven activation of LGR5 in colorectal cancer.Nature communications · 2026Article
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- Article
- Increased expression of a subset of genes within reduced copy number regions across multiple cancer types.bioRxiv : the preprint server for biology · 2026Article
- Enhancer reprogramming: critical roles in cancer and promising therapeutic strategies.Cell death discovery · 2025Review
- STC2 promotes anoikis resistance by modulating TGIF1 mRNA stability in colorectal cancer.Frontiers in cell and developmental biology · 2025Article
- SE-lncRNAs in Cancer: Classification, Subcellular Localisation, Function and Corresponding TFs.Journal of cellular and molecular medicine · 2024Review
- Effects of super-enhancers in cancer metastasis: mechanisms and therapeutic targets.Molecular cancer · 2024Review
- Transcription factor EHF interacting with coactivator AJUBA aggravates malignancy and acts as a therapeutic target for gastroesophageal adenocarcinoma.Acta pharmaceutica Sinica. B · 2024Article
- [Effect of CircCCND1 on the Malignant Biological Behaviors of H446 Lung Cancer Cells by Regulating the MiR-340-5p/TGIF1 Axis].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024Article
- Super-Enhancers and Their Parts: From Prediction Efforts to Pathognomonic Status.International journal of molecular sciences · 2024Review
- Pathogenic role of super-enhancers as potential therapeutic targets in lung cancer.Frontiers in pharmacology · 2024Review
- NF-κB subunits direct kinetically distinct transcriptional cascades in antigen receptor-activated B cells.Nature immunology · 2023Article
- The super-enhancer-driven lncRNA LINC00880 acts as a scaffold between CDK1 and PRDX1 to sustain the malignance of lung adenocarcinoma.Cell death & disease · 2023Article
- Super-enhancers complexes zoom in transcription in cancer.Journal of experimental & clinical cancer research : CR · 2023Review
- Oncogenic super-enhancers in cancer: mechanisms and therapeutic targets.Cancer metastasis reviews · 2023Review
- An integrative epigenomic approach identifies ELF3 as an oncogenic regulator in ASCL1-positive neuroendocrine carcinoma.Cancer science · 2023Article
- Lung Cancer through Transcription Factors.International journal of molecular sciences · 2023Article
- Superenhancer activation of KLHDC8A drives glioma ciliation and hedgehog signaling.The Journal of clinical investigation · 2023Article
- The Emerging Role of Super-enhancers as Therapeutic Targets in The Digestive System Tumors.International journal of biological sciences · 2023Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung adenocarcinoma (LUAD) relies on dysregulated gene expression to sustain its infinite growth and progression. Emerging evidence indicates that aberrant transcriptional program results from core transcriptional regulatory circuitry (CRC) which is driven by super-enhancers (SEs). In this study, by integrating profiles of H3K27Ac chromatin immunoprecipitation sequencing (ChIP-seq) from normal adult lung and LUAD cell lines, we revealed that widespread alterations of the super-enhancer were presence during lung carcinogenesis. With SE-based modeling of regulatory circuits and assessments of transcription factor (TF) dependencies, we reconstructed an interconnected transcriptional regulation network formed by three master TFs, including ELF3, EHF, and TGIF1, all of which promoted each other's expression that confirmed by ChIP-qPCR and western blot. Loss-of function assay revealed that each of them is essential for LUAD cells survival, invasion and metastasis. Meanwhile, the rescue assay also illustrated the transacting transcriptional regulatory circuitry. In addition, the mRNA levels of ELF3, EHF, and TGIF1 were differentially expressed in LUAD tumors and peritumoral tissue. IHC of serial sections revealed that high expressions of CRC (ELF3/EHF/TGIF1-High) were closely associated with high proliferative activity in tumor tissue and poor prognosis on patients with LUAD. Finally, we used small molecular inhibitors to perturb the transcriptional circuitry, also exhibited a prominent anti-cancer effect in vitro. Our findings reveal the mechanism of the transcriptional dysregulation and addiction of LUAD.
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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.