ArticleCancer research2019
Epigenomic Profiling Discovers Trans-lineage SOX2 Partnerships Driving Tumor Heterogeneity in Lung Squamous Cell Carcinoma.
Article in Cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- The Role of Alternative Splicing in Lung Cancer: Mechanisms, Regulators, and Therapeutic Implications.International journal of molecular sciences · 2026Review
- The expression landscape and clinical significance of cancer-specific RNA transcripts across human cancers.Journal of translational medicine · 2026Article
- Vascular STING activation facilitates NK cell anti-tumor immunity in small cell lung cancer.Cancer cell · 2026Article
- TP63 mediates the generation of tumour-specific chromatin loops that underlie MYC activation in radiation-induced tumorigenesis.Nature communications · 2025Article
- SOX2 utilizes FOXA1 as a heteromeric transcriptional partner to drive proliferation in therapy-resistant prostate cancer.bioRxiv : the preprint server for biology · 2025Article
- Enhancer reprogramming: critical roles in cancer and promising therapeutic strategies.Cell death discovery · 2025Review
- Targeting TREX1 Induces Innate Immune Response in Drug-Resistant Small-Cell Lung Cancer.Cancer research communications · 2024Article
- SOX2 interacts with hnRNPK to modulate alternative splicing in mouse embryonic stem cells.Cell & bioscience · 2024Article
- KLF7 regulates super-enhancer-driven IGF2BP2 overexpression to promote the progression of head and neck squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2024Article
- Pathogenic role of super-enhancers as potential therapeutic targets in lung cancer.Frontiers in pharmacology · 2024Review
- Epigenetic reprogramming of a distal developmental enhancer cluster drives SOX2 overexpression in breast and lung adenocarcinoma.Nucleic acids research · 2023Article
- Transcriptional Circuitry of NKX2-1 and SOX1 Defines an Unrecognized Lineage Subtype of Small-Cell Lung Cancer.American journal of respiratory and critical care medicine · 2022Article
- Self-restricted circular RNA circSOX2 suppressed the malignant progression in SOX2-amplified LUSC.Cell death & disease · 2022Article
- Single-cell transcriptional regulation and genetic evolution of neuroendocrine prostate cancer.iScience · 2022Article
- A predominant enhancer co-amplified with the SOX2 oncogene is necessary and sufficient for its expression in squamous cancer.Nature communications · 2021Article
- Intrinsic Immunogenicity of Small Cell Lung Carcinoma Revealed by Its Cellular Plasticity.Cancer discovery · 2021Article
- Alternate Roles of Sox Transcription Factors beyond Transcription Initiation.International journal of molecular sciences · 2021Review
- Super enhancers-Functional cores under the 3D genome.Cell proliferation · 2021Review
- Prototypical oncogene family Myc defines unappreciated distinct lineage states of small cell lung cancer.Science advances · 2021Article
- Chromatin Looping Shapes KLF5-Dependent Transcriptional Programs in Human Epithelial Cancers.Cancer research · 2020Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
Molecular characterization of lung squamous cell carcinoma (LUSC), one of the major subtypes of lung cancer, has not sufficiently improved its nonstratified treatment strategies over decades. Accumulating evidence suggests that lineage-specific transcriptional regulators control differentiation states during cancer evolution and underlie their distinct biological behaviors. In this study, by investigating the super-enhancer landscape of LUSC, we identified a previously undescribed "neural" subtype defined by Sox2 and a neural lineage factor Brn2, as well as the classical LUSC subtype defined by Sox2 and its classical squamous partner p63. Robust protein-protein interaction and genomic cooccupancy of Sox2 and Brn2, in place for p63 in the classical LUSC, indicated their transcriptional cooperation imparting this unique lineage state in the "neural" LUSC. Forced expression of p63 downregulated Brn2 in the "neural" LUSC cells and invoked the classical LUSC lineage with more squamous/epithelial features, which were accompanied by increased activities of ErbB/Akt and MAPK-ERK pathways, suggesting differential dependency. Collectively, our data demonstrate heterogeneous cell lineage states of LUSC featured by Sox2 cooperation with Brn2 or p63, for which distinct therapeutic approaches may be warranted. SIGNIFICANCE: Epigenomic profiling reveals a novel subtype of lung squamous cell carcinoma with neural differentiation.
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