Project description:This study was designed to identify genes aberrantly expressed in esophageal squamous cell carcinoma (ESCC) cells. Three esophageal squamous cell carcinoma-derived cell lines and one normal human esophageal squamous cell line were analyzed.
Project description:We obtained transcriptome profiling (RNA-seq) of human esophageal squamous cell carcinoma cell line KYSE150 stabley transfected clones with pIRES2-EGFP vector or human NCCRP1-expression vector by using next generation sequencing.
Project description:We obtained transcriptome profiling (RNA-seq) of human esophageal squamous cell carcinoma cell line KYSE30 cells stabley transfected with pIRES2-EGFP vector or human RHCG-expression vector by using next generation sequencing.
Project description:We have mapped binding sites for the histone demethylase, JMJD2C/KDM4C/GASC1, and the effect of JMJD2C depletion on H3K9me3 and H3K36me3 distributions in KYSE150 cells. The human esophageal carcinoma cell line, KYSE150, contains an amplification of the JMJD2C locus. ChIP-seq was performed using chromatin from control or JMJD2C-depleted KYSE150 cells and antibodies recognizing JMJD2C, H3K4me3, H3K9me3 or H3K36me3.
Project description:To reveal the modified gene regulatory elements including transcription factors and enhancers in esophageal squamous carcinoma cells (ESCC), we performed Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq) with two ESCC cell lines, i.e. KYSE-30 and KYSE-150, and a non-cancerous esophageal epithelial cell line, HET-1A. This data showed that hyper-accessible regions in ESCC cells contained genes related with cancer hallmarks including DNA replication and angiogenesis. Further motif analysis suggested that AP-1 family transcription factors bind the hyper-accessible regions in KYSE-30 cells as compared to those in HET-1A cells.
Project description:Profiles of esophageal squamous cell carcinoma and normal esophageal normal epithelium normal cell line. Analysis provides validation of novel microRNA targets prediction algorithms. esophageal squamous cell carcinoma:14, normal epithelium cell:2
Project description:Purpose: Next Generation sequencing (NGS) has revolutionized system-based cellular pathway analysis. The purpose of this study was to conduct RNA-SEQ analysis after knocking down the gene MAFB in human esophageal squamous cell carcinoma cell line KYSE450 to observe the expression changes of the transcriptome genes
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.
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.
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.
