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Master TFs bind SOEs to drive tumorigenesis in LUSC cells [ChIP-seq]

ABSTRACT: These SOEs were highly enriched for H3K27ac signals in H520/HCC95 cells. Binding of key TFs, also known as mater regulators, is usually enriched in cell fate determinant or disease-specific cis-regulatory elements, such as super-enhancers.To find out which TFs were essential for the tumorigenesis of LUSC, sequence motif enrichment analysis was performed in SOE using all CDE as background. As expected, the well-established master TFs of LUSC, i.e., SOX2 and TP63, exhibited the highest enrichment of binding sites among all tested TFs .To confirm their binding in SOEs, we performed ChIP-seq for these factors, including p63, SOX2, GRHL2 and KLF5, all of which exhibited significant and specific binding to most SOEs, compared to other non-SOE genomic regions.

ORGANISM(S): Homo sapiens

PROVIDER: GSE293731 | GEO | 2025/09/02

REPOSITORIES: GEO

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Project description:Lung squamous cell carcinoma (LUSC) is associated with poor survival owing to the lack of advanced targeted therapies, due to the incomplete characterization of complex genetic profiles. Therefore, it is essential to elucidate the molecular mechanisms of LUSC via the mice model and human database to understand the LUSC pathogenesis. A LUSC BALB/c mice model was established using N-nitroso-tris-chloroethylurea (NTCU). After termination of mice, the lung tissues were subjected to RNA sequencing. First, DESeq2 was used to normalize the read count, followed by gene set enrichment analysis (GSEA) to identify the affected pathways in LUSC. Subsequently, the pathogenic single nucleotide polymorphism (SNP) was determined using Protein Variation Effect Analyzer (PROVEAN) and Sorting Intolerant From Tolerant (SIFT), following scores of < 0.05 and < -2.5, respectively, which were then functionally enriched using g:Profiler. The transcriptomic profile of human LUSC patients was obtained from The International Cancer Genome Consortium (ICGC) and analyzed. The impact of pathogenic simple somatic mutation in human LUSC was determined using the Combined Annotation Dependent Depletion (CADD) score, which was functionally enriched using g:Profiler. Additionally, the enriched pathway of LUSC patients with complete remission (responsive) was compared with those with disease progression or deceased (non-responsive) post-GSEA treatment. All pathway analysis was possibly referred to the Reactome database, and an adjusted p-value < 0.05 was considered statistically significant. Based on the transcriptomic analysis of LUSC mice, the top pathway enriched from the animal study and human LUSC revealed similarity in four major themes: cholesterol, cellular interaction, immune, and extracellular matrix dysregulation. Furthermore, the overrepresented pathways identified in LUSC patients were consistent with the four major themes dysregulated in LUSC tumors. This study identified several biological pathways that may contribute to LUSC development and potential targets for future LUSC therapy.

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Master TFs bind SOEs to drive tumorigenesis in LUSC cells [ChIP-seq]

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