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Super-enhancer-driven CCAT1 is co-activated by SOX2 and TP63 and promotes squamous cancer from esophagus, head and neck and lung [ChIP-seq]

ABSTRACT: Super-enhancer-driven CCAT1 is co-activated by SOX2 and TP63 and promotes squamous cancer from esophagus, head and neck and lung [ChIP-seq]

PROVIDER: PRJNA417252 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6260740.fastq.gz	Fastqsanger.gz
	SRR6260731.fastq.gz	Fastqsanger.gz
	SRR6260732.fastq.gz	Fastqsanger.gz
	SRR6260733.fastq.gz	Fastqsanger.gz
	SRR6260734.fastq.gz	Fastqsanger.gz

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Super-enhancer-driven CCAT1 is co-activated by SOX2 and TP63 and promotes squamous cancer from esophagus, head and neck and lung [RNA-seq]

Project description:Squamous cell carcinomas (SCCs) are aggressive malignancies. Previous report demonstrated that the transcription factors TP63 and SOX2 exhibited overlapping genomic occupancy in SCCs. Our recent study have identified TP63 and SOX2 as super-enhancer-associated genes. However, functional consequences of their frequent co-localization at super-enhancers region remains unexplored. Here, ChIP-seq result indicated TP63 and SOX2 co-occupied peaks are significantly located the super enhancer region compare with unique of TP63 and SOX2 signaling, and combined RNA-seq analyses of different types of SCCs reveal that TP63 and SOX2 cooperatively regulate expression of the super-enhancer-associated the long non-coding RNA (lncRNA) gene, CCAT1. CCAT1 is highly expressed in SCCs compared to either other tumor types or normal tissues. CCAT1 expression strongly correlates with expression levels of TP63 and SOX2. Silencing of CCAT1 significantly reduces cellular growth both in vitro and in vivo, phenotyping the effect of silencing either TP63 or SOX2. Furthermore, ChIP-Seq and luciferase reporter assays demonstrate TP63 and SOX2 co-occupy the promoter and super-enhancer regions of CCAT1. Interaction of CCAT1 with TP63 and SOX2 are validated by RNA immunoprecipitation. In addition, ChIRP analysis suggests that CCAT1 regulates EGFR expression by binding to the super-enhancer of EGFR. Further investigations shows that CCAT1 activates both the MEK/ERK1/2 and PI3K/AKT signaling pathways through up-regulation of EGFR. In conclusion, CCAT1 is driven by master transcription factors TP63 and SOX2 and is recruited to the super-enhancer of EGFR, promoting SCC tumorigenesis through activation of the MEK/ERK1/2 and PI3K/AKT signaling pathways. These studies help to explain the pathogenesis of SCC and aids in providing novel therapeutic strategy.

2018-09-17 | GSE106564 | GEO

Super-enhancer-driven CCAT1 is co-activated by SOX2 and TP63 and promotes squamous cancer from esophagus, head and neck and lung [ChIP-seq]

2018-09-17 | GSE106563 | GEO

Super-enhancer-driven CCAT1 is co-activated by SOX2 and TP63 and promotes squamous cancer from esophagus, head and neck and lung

Project description:Super-enhancer-driven CCAT1 is co-activated by SOX2 and TP63 and promotes squamous cancer from esophagus, head and neck and lung

| PRJNA417249 | ENA

Super-enhancer-driven CCAT1 is co-activated by SOX2 and TP63 and promotes squamous cancer from esophagus, head and neck and lung [RNA-seq]

Project description:Super-enhancer-driven CCAT1 is co-activated by SOX2 and TP63 and promotes squamous cancer from esophagus, head and neck and lung [RNA-seq]

| PRJNA417255 | ENA

Super-enhancer-driven CCAT1 is co-activated by SOX2 and TP63 and promotes squamous cancer from esophagus, head and neck and lung

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-09-17 | GSE106565 | GEO

Differential gene expression by suppression of either SOX2 or TP63 in KYSE70 human esophageal squamous carcinoma cell line.

Project description:SOX2 is a transcription factor essential for pluripotent stem cells, and development and maintenance of squamous epithelium. We previously reported SOX2 an oncogene subject to highly recurrent genomic amplification in squamous cell carcinomas (SCCs)1. Here we demonstrate in SCCs that SOX2 interacts with another master squamous transcription factor p63, and through ChIP-seq show that genomic occupancy of SOX2 overlaps with that of p63 at a large number of loci and that they cooperatively regulate gene expression including ETV4, which we find essential for SOX2-amplified SCC cell survival. Furthermore, SOX2 binds to distinct genomic loci in SCCs than in embryonic stem cells and the SOX2-p63 coordinate binding is unique to SCC. In addition, a subset of SOX2 genomic binding sites in SCC that lack p63 co-occupancy are co-occupied by the AP-1 transcriptional complex. These demonstrate that SOX2M-bM-^@M-^Ys actions in SCC differ substantially from its role in pluripotency and identify novel SOX2 interactions that will enable deeper characterization of SOX2M-bM-^@M-^Ys function in SCC. KYSE70 cells with stable expression of either pLKO-Tet-Op-shSOX2 or pLKO-Tet-Op-shTp63 were treated with 50ng/ml of doxycyline for 4 days. Total RNA was extracted, polyA+ selected, reverse transcribed, library constructed and sequencing was performed with Illumina HiSeq 2000. Differencial gene expression between the stable cell lines with Dox-induced and non-Dox treated was analyzed to determine the effects by suppression of either SOX2 or TP63 in KYSE70 cells.

2014-05-13 | E-GEOD-47058 | biostudies-arrayexpress

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Project description:Barrett's esophagus transcriptome was analysed and compared with Barrett's esophagus primary cell culture and esophageal adenocarcinoma. Keywords: SAGE analysis to compare tissues Barrett's esophagus biopsy was taken from 1 male metaplastic Barrett's esophagus patient. Barrett's esophagus primary cell culture was cultures from a biopsy taken from a Barrett's esophagus patient and cultured for about 4 to 5 weeks. Esophageal adenocarcinoma was taken from a patient known to have cancer and previously Barrett's esophagus

2006-06-28 | E-GEOD-5155 | biostudies-arrayexpress

Co-activation of super-enhancer-driven CCAT1 by TP63 and SOX2 promotes squamous cancer progression.

Project description:Squamous cell carcinomas (SCCs) are aggressive malignancies. Previous report demonstrated that master transcription factors (TFs) TP63 and SOX2 exhibited overlapping genomic occupancy in SCCs. However, functional consequence of their frequent co-localization at super-enhancers remains incompletely understood. Here, epigenomic profilings of different types of SCCs reveal that TP63 and SOX2 cooperatively and lineage-specifically regulate long non-coding RNA (lncRNA) CCAT1 expression, through activation of its super-enhancers and promoter. Silencing of CCAT1 substantially reduces cellular growth both in vitro and in vivo, phenotyping the effect of inhibiting either TP63 or SOX2. ChIRP analysis shows that CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR expression by binding to the super-enhancers of EGFR, thereby activating both MEK/ERK1/2 and PI3K/AKT signaling pathways. These results together identify a SCC-specific DNA/RNA/protein complex which activates TP63/SOX2-CCAT1-EGFR cascade and promotes SCC tumorigenesis, advancing our understanding of transcription dysregulation in cancer biology mediated by master TFs and super-enhancers.

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Identification the Expression of Sox2 in Colorectal Cancer Tissues

Project description:Sox2 has been studied in several types of human solid tumors. The investigators found that Sox2 had higher expression level in colorectal cancer and metastatic tissues than normal tissues. So the investigators assumed that whether Sox2 plays an important role in the progression and migration of colon cancer.

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Squamous esophagus

Project description:SAGE libraries made of squamous esophagus tissue, primary cell culture or esophageal squamous cell carcinoma Keywords: SAGE analysis of different tissues squamous esophagus biopsy was taken from 1 male metaplastic Barrett's esophagus patient. primary cell culture was from 1 male Barrett's esophagus patient. Esophageal squamous cell carcinoma was from a patient known to have ESCC

2006-06-28 | E-GEOD-5154 | biostudies-arrayexpress

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