ArticleNucleic acids research2021
Activation of bivalent factor DLX5 cooperates with master regulator TP63 to promote squamous cell carcinoma.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Environmental Lead Promotes Breast Cancer Migration and Invasion via the AKR1C3-NF-κB-MMP Axis.Biomedicines · 2026Article
- TP63 regulates pyroptosis via NF-κB/NLRP3/caspase-1 signaling in interstitial cystitis: insights from single-cell sequencing.Open medicine (Warsaw, Poland) · 2026Article
- Enhancing the Efficacy, Utility, and Throughput of the Transcription Block Survival Peptide Library Screening Platform.JACS Au · 2025Article
- Interplay and cooperation between GLI2 and master transcription factors promote progression of esophageal squamous cell carcinoma.American journal of human genetics · 2025Article
- 101 Machine Learning Algorithms for Mining Esophageal Squamous Cell Carcinoma Neoantigen Prognostic Models in Single-Cell Data.International journal of molecular sciences · 2025Article
- Melatonin attenuates degenerative disc degression by downregulating DLX5 via the TGF/Smad2/3 pathway in nucleus pulposus cells.JOR spine · 2024Article
- New direction: identification of immunoinflammatory subtypes and potential therapeutic targets for cholangiocarcinoma.Discover oncology · 2024Article
- The TDP-43/TP63 Positive Feedback Circuit Promotes Esophageal Squamous Cell Carcinoma Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Activation of Bivalent Gene POU4F1 Promotes and Maintains Basal-like Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Predicting mechanism of immune response in microsatellite instability colorectal cancer.Heliyon · 2024Article
- Somatic mutations in four novel genes contribute to homologous recombination deficiency in breast cancer: a real-world clinical tumor sequencing study.The journal of pathology. Clinical research · 2024Article
- DNA methylation-activated full-length EMX1 facilitates metastasis through EMX1-EGFR-ERK axis in hepatocellular carcinoma.Cell death & disease · 2023Article
- SHFM1 deficiency suppresses esophageal squamous cell carcinomas progression via modulating NF‑κB signaling and enhancing nature killer cell‑mediated tumor surveillance.Experimental and therapeutic medicine · 2023Article
- Article
- Upregulated YTHDF1 associates with tumor immune microenvironment in head and neck squamous cell carcinomas.Translational cancer research · 2022Article
- Analyzing integrated network of methylation and gene expression profiles in lung squamous cell carcinoma.Scientific reports · 2022Article
- Comprehensive 3D epigenomic maps define limbal stem/progenitor cell function and identity.Nature communications · 2022Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To reconstruct systematically hyperactive transcription factor (TF)-dependent transcription networks in squamous cell carcinomas (SCCs), a computational method (ELMER) was applied to 1293 pan-SCC patient samples, and 44 hyperactive SCC TFs were identified. As a top candidate, DLX5 exhibits a notable bifurcate re-configuration of its bivalent promoter in cancer. Specifically, DLX5 maintains a bivalent state in normal tissues; its promoter is hypermethylation, leading to DLX5 transcriptional silencing in esophageal adenocarcinoma (EAC). In stark contrast, DLX5 promoter gains active histone marks and becomes transcriptionally activated in ESCC, which is directly mediated by SOX2. Functionally, silencing of DLX5 substantially inhibits SCC viability both in vitro and in vivo. Mechanistically, DLX5 cooperates with TP63 in regulating ∼2000 enhancers and promoters, which converge on activating cancer-promoting pathways. Together, our data establish a novel and strong SCC-promoting factor and elucidate a new epigenomic mechanism - bifurcate chromatin re-configuration - during cancer development.
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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.