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TP63-driven super-enhancer-associated LINC01503 promotes the malignancy of esophageal squamous cell carcinoma (ChIP-Seq)

ABSTRACT: TP63-driven super-enhancer-associated LINC01503 promotes the malignancy of esophageal squamous cell carcinoma (ChIP-Seq)

PROVIDER: PRJNA416868 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6246080.fastq.gz	Fastqsanger.gz
	SRR6246081.fastq.gz	Fastqsanger.gz
	SRR6246072.fastq.gz	Fastqsanger.gz
	SRR6246082.fastq.gz	Fastqsanger.gz
	SRR6246073.fastq.gz	Fastqsanger.gz

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TP63-driven super-enhancer-associated LINC01503 promotes the malignancy of esophageal squamous cell carcinoma

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TP63-driven super-enhancer-associated LINC01503 promotes the malignancy of esophageal squamous cell carcinoma (4C-Seq)

Project description:TP63-driven super-enhancer-associated LINC01503 promotes the malignancy of esophageal squamous cell carcinoma (4C-Seq)

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Epigenetic regulation of p63 blocks squamous-to-neuroendocrine transdifferentiation in esophageal development and malignancy [RNAseq_ip63]

Project description:While cell fate determination and maintenance are important in establishing and preserving tissue identity and function during development, aberrant cell fate transition leads to cancer cell heterogeneity and resistance to treatment. Here, we report an unexpected role for the transcription factor p63 (Trp63/TP63) in the fate choice of squamous versus neuroendocrine lineage in esophageal development and malignancy. Deletion of p63 results in extensive neuroendocrine differentiation in the developing mouse esophagus and esophageal progenitors derived from human embryonic stem cells. In human esophageal neuroendocrine carcinoma (eNEC) cells, p63 is transcriptionally silenced by EZH2-mediated H3K27 trimethylation (H3K27me3). Upregulation of the major p63 isoform ΔNp63α, through either ectopic expression or EZH2 inhibition, promotes squamous transdifferentiation of eNEC cells. Together these findings uncover p63 as a rheostat in coordinating the transition between squamous and neuroendocrine cell fates during esophageal development and tumor progression.

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Epigenetic regulation of p63 blocks squamous-to-neuroendocrine transdifferentiation in esophageal development and malignancy [RNAseq_Ezh2i]

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Epigenetic regulation of p63 blocks squamous-to-neuroendocrine transdifferentiation in esophageal development and malignancy [RNAseq_Eso]

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Epigenetic regulation of p63 blocks squamous-to-neuroendocrine transdifferentiation in esophageal development and malignancy [CUTnTag_ip63]

2024-07-26 | GSE242437 | GEO

Epigenetic regulation of p63 blocks squamous-to-neuroendocrine transdifferentiation in esophageal development and malignancy [CUTnTag_Ezh2i]

2024-07-26 | GSE242436 | GEO

TP63-driven super-enhancer-associated LINC01503 promotes the malignancy of esophageal squamous cell carcinoma (ChIP-Seq)

Project description:Background & Aims: Lineage-specific expression of long non-coding RNAs (lncRNAs) has been observed recently. However, the underlying mechanism of such specific transcription regulation is unclear. The aim of this study is to identify squamous cell carcinoma (SCC) lineage-specific lncRNAs and to investigate the mechanisms for their expression and function. Methods: Expression characteristics and functions of four candidate SCC-specific lncRNAs were explored. qRT-PCR assays were employed to measure the expression of LINC01503 in 113 tumor/normal matched esophageal SCC (ESCC) cases and its association with survival was determined. The mechanisms underlying LINC01503 function and regulation in ESCC cells were examined using molecular biological methods. Results: Using SCC as a model, we identified a novel super-enhancer (SE)-driven lncRNA, LINC01503, which was uniquely expressed in SCCs such as those from esophagus (ESCC) and head and neck (HNSC). LINC01503 was up-regulated in SCCs and its high expression correlated with poor clinical outcomes. SCC master transcriptional factor TP63 directly bound to a SE at LINC01503 locus and activated its transcription. LINC01503 exhibited strong oncogenic functions in ESCC cell models both in vitro and in vivo. ERK2 and EBP-1 were identified as interacting proteins mediating the effects of LINC01503. Specifically, LINC01503 protected ERK2 from dephosphorylation by DUSP-6, leading to the activation of ERK/MAPK pathway. Similarly, LINC01503 interfered the interaction between EBP-1 and PI3K p85, enhancing Akt signaling pathway. Conclusions: These results demonstrated that LINC01503 is a lineage-specific oncogene in ESCC, which may serve as a potential biomarker and therapeutic target for SCC patients.

2018-12-01 | GSE106433 | GEO