ArticleNature communications2018
BCL11A interacts with SOX2 to control the expression of epigenetic regulators in lung squamous carcinoma.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 85 citations in OpenAlex.
- Gene dependency-informed inference of response to targeted cancer therapies.Nature communications · 2026Article
- Research Advances and Disease Modeling in Respiratory Organoids.Biomedicines · 2026Review
- Differences between lung adenocarcinoma and lung squamous cell carcinoma: Driver genes, therapeutic targets, and clinical efficacy.Genes & diseases · 2025Review
- Airway basal stem cell therapy for lung diseases: an emerging regenerative medicine strategy.Stem cell research & therapy · 2025Review
- Review
- Wemics: A Single-Base Resolution Methylation Quantification Method for Enhanced Prediction of Epigenetic Regulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Integrated bulk and single-cell transcriptomes reveal pyroptotic signature in prognosis and therapeutic options of hepatocellular carcinoma by combining deep learning.Briefings in bioinformatics · 2023Article
- Refphase: Multi-sample phasing reveals haplotype-specific copy number heterogeneity.PLoS computational biology · 2023Article
- Transcription Factor BCL11A Regulates Schwann Cell Behavior During Peripheral Nerve Regeneration.Molecular neurobiology · 2023Article
- RNA-seq analysis reveals candidate genes associated with proliferation, invasion, and migration in BCL11A knockdown B-NHL cell lines.Annals of hematology · 2023Article
- Intratumoral Microbiota-Host Interactions Shape the Variability of Lung Adenocarcinoma and Lung Squamous Cell Carcinoma in Recurrence and Metastasis.Microbiology spectrum · 2023Article
- BCL11A Expression in Non-Small Cell Lung Cancers.International journal of molecular sciences · 2023Article
- Identification of a genomic DNA sequence that quantitatively modulates KLF1 transcription factor expression in differentiating human hematopoietic cells.Scientific reports · 2023Article
- Construction and validation of a tumor mutational burden and immune-related prognostic model for predicting the prognosis of patients with lung squamous cell carcinoma.Journal of thoracic disease · 2023Article
- Differential Expression Enrichment Tool (DEET): an interactive atlas of human differential gene expression.NAR genomics and bioinformatics · 2023Article
- The Tumorigenic Effect of the High Expression of Ladinin-1 in Lung Adenocarcinoma and Its Potential as a Therapeutic Target.Molecules (Basel, Switzerland) · 2023Article
- The DNA repair function of BCL11A suppresses senescence and promotes continued proliferation of triple-negative breast cancer cells.NAR cancer · 2022Article
- Article
- Signaling pathways and targeted therapies in lung squamous cell carcinoma: mechanisms and clinical trials.Signal transduction and targeted therapy · 2022Review
- BCL11A promotes myeloid leukemogenesis by repressing PU.1 target genes.Blood advances · 2022Article
Corrections and comments
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Authors and funding
20 authors at 6 institutions in 2 countries.
Funding
Abstract
Patients diagnosed with lung squamous cell carcinoma (LUSC) have limited targeted therapies. We report here the identification and characterisation of BCL11A, as a LUSC oncogene. Analysis of cancer genomics datasets revealed BCL11A to be upregulated in LUSC but not in lung adenocarcinoma (LUAD). Experimentally we demonstrate that non-physiological levels of BCL11A in vitro and in vivo promote squamous-like phenotypes, while its knockdown abolishes xenograft tumour formation. At the molecular level we found that BCL11A is transcriptionally regulated by SOX2 and is required for its oncogenic functions. Furthermore, we show that BCL11A and SOX2 regulate the expression of several transcription factors, including SETD8. We demonstrate that shRNA-mediated or pharmacological inhibition of SETD8 selectively inhibits LUSC growth. Collectively, our study indicates that BCL11A is integral to LUSC pathology and highlights the disruption of the BCL11A-SOX2 transcriptional programme as a novel candidate for drug 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.