ArticleNature communications2021
Transcriptional super-enhancers control cancer stemness and metastasis genes in squamous cell carcinoma.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.
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Who cites it
84 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.
- Bibliometric analysis of evolutionary trends and hotspots of super-enhancers in cancer.Frontiers in pharmacology · 2023Pooled it
- Super-enhancer landscape regulated by CDK12 drives retinoblastoma progression.British journal of cancer · 2026Article
- Targeting MDA-9/syntenin-1 (SDCBP) as a strategy to eliminate head and neck squamous cell carcinoma stem cells.Cancer letters · 2026Article
- Rewiring Cellular Context as A Central Mechanism Governing Cancer Stem Cell Survival: Insights from ESC Comparisons.Stem cell reviews and reports · 2026Review
- 3D chromatin architecture in cancer: mechanisms of dysregulation and emerging therapeutic strategies.Experimental & molecular medicine · 2026Review
- Disrupting MED8-dependent epigenetic reprogramming augments avapritinib sensitivity in PDGFRA-driven glioma.Journal of experimental & clinical cancer research : CR · 2026Article
- Understanding super enhancers in genome architecture and their roles in livestock breeding.BMC genomics · 2026Review
- BRD2 upregulation as a pan-cancer adaptive resistance mechanism to BET inhibition.Cellular & molecular biology letters · 2026Article
- Multi-omics evaluation of cell lines as models for metastatic prostate cancer.Communications biology · 2026Article
- From Environmental Risk to Cancer Stemness: Epigenetic Regulation in Oral Squamous Cell Carcinoma.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Article
- Targeting pre-existing club-like cells in prostate cancer potentiates androgen deprivation therapy.EMBO molecular medicine · 2026Article
- Cancer stem cell heterogeneity‑inspired therapeutics for enhancing tumor treatment outcomes (Review).International journal of oncology · 2026Review
- Role of the Super-Enhancer Component Bromodomain Protein 4 in the Radiation Response of Human Head and Neck Squamous Cell Carcinoma Cells.Current issues in molecular biology · 2026Article
- LUCAT1 promotes stemness in head and neck squamous cell carcinoma by sponging miR-128.Frontiers in oncology · 2026Article
- Multi-omics investigation of perineural invasion in head and neck squamous cell carcinoma: neuroimmune mechanisms and clinical implications.Frontiers in immunology · 2026Article
- A Single Cell Atlas of the COPD Lung Identifies Inflammatory Reprogramming in Fibroblasts.International journal of chronic obstructive pulmonary disease · 2026Article
- A novel super-enhancer-driven lncRNA LINC00973 governs head and neck squamous cell carcinoma progression through EN2.Cell death & disease · 2025Article
- Systems pharmacology approaches decipher the anti-cancer efficacy of ethnopharmacological agents in hepatocellular carcinoma.Scientific reports · 2025Article
- A patient-derived orthotopic xenograft model unveils metastatic dynamics in head and neck squamous cell carcinoma.The FEBS journal · 2025Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Cancer stem cells (CSCs) play a critical role in invasive growth and metastasis of human head and neck squamous cell carcinoma (HNSCC). Although significant progress has been made in understanding the self-renewal and pro-tumorigenic potentials of CSCs, a key challenge remains on how to eliminate CSCs and halt metastasis effectively. Here we show that super-enhancers (SEs) play a critical role in the transcription of cancer stemness genes as well as pro-metastatic genes, thereby controlling their tumorigenic potential and metastasis. Mechanistically, we find that bromodomain-containing protein 4 (BRD4) recruits Mediators and NF-κB p65 to form SEs at cancer stemness genes such as TP63, MET and FOSL1, in addition to oncogenic transcripts. In vivo lineage tracing reveals that disrupting SEs by BET inhibitors potently inhibited CSC self-renewal and eliminated CSCs in addition to elimination of proliferating non-stem tumor cells in a mouse model of HNSCC. Moreover, disrupting SEs also inhibits the invasive growth and lymph node metastasis of human CSCs isolated from human HNSCC. Taken together, our results suggest that targeting SEs may serve as an effective therapy for HNSCC by eliminating CSCs.
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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.