Divergent functions of master TFs in LUSC [RNA-seq]
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ABSTRACT:
PROVIDER: PRJNA1246124 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To examine the essential role of these four TFs particularly the two novel ones KLF5 and GRHL2, we depleted individual factors with siRNA in a human LUSC cell line HCC95. The results consistently showed that cells deficient of any of these 4 factors except SOX2 were revealed with most prominent deficiency in epidermal cell development which is important features of LUSC development . Note that SOX2 is known also to play a primary role in neuron development, and the depletion indeed caused disturbance in regulation of nervous system development. The pathways involved in epidermal cell development involving regulating keratinization and epithelial-mesenchymal transition influencing tumor behavior, aggressiveness, and response to treatment.
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Project description: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.
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Project description:Master TFs bind SOEs to drive tumorigenesis in LUSC cells [ChIP-seq]
| PRJNA1246122 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
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Project description:Cyclin-dependent kinase 5 regulatory subunit associated protein 3(CDK5RAP3) is regulated by master TFs in neuroblastoma, and its functions in neuroblastoma are yet unclear. Herein, we observed a significantly elevated CDK5RAP3 expression level in neuroblastoma, which was associated with a poor prognosis in patients. CDK5RAP3 promotes the growth of neuroblastoma cells both in vitro and in vivo. Mechanistically, defective CDK5RAP3 interferes with UFMylation system, thereby triggering endoplasmic reticulum(ER)-Phagy. Additionally, we provide evidence that CDK5RAP3 maintains stability of MEIS2, a master TF in neuroblastoma, and in turn contributes high expression of CDK5RAP3. Overall, our findings shed light on the molecular mechanisms through which CDK5RAP3 promotes tumor progression and suggest that its inhibition may represent a novel therapeutic strategy in neuroblastoma.
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Project description:CDK5RAP3 is activated by master TFs and regulates ER-Phagy in neuroblastoma
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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.
2024-12-31 | GSE240837 | GEO
Project description:TCGA Analysis of DNA Methylation for LUSC using Illumina Infinium HumanMethylation450 platform EXP-598 Assay Type: Methylation Provider: Illumina Array Designs: jhu-usc.edu_TCGA_HumanMethylation450 Organism: Homo sapiens (ncbitax) Tissue Sites: Lung Material Types: Control Analyte, Solid normal_tissue, organism_part, Primary solid_tumor Disease States: Lung Squamous Cell Carcinoma, NOT SPECIFIED
2015-05-14 | E-GEOD-68825 | biostudies-arrayexpress
Project description:BCL11A is upregulated in lung squamous cell carcinoma (LUSC) but not in lung adenocarcinoma (LUAD). BCL11A interacts with SOX2 at protein level. ChIP-Seq experiment was performed for BCL11A and SOX2 in LUSC LK-2 control or BCL11A-KD cell line in order to identify their role in LUSC pathology.
2018-07-05 | E-MTAB-6958 | biostudies-arrayexpress