Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA382285 | ENA |
REPOSITORIES: ENA
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Project description:The objective was to investigate the toxic effect of Bortezomib on human esophageal carcinoma epithelial cells at gene expression level. Gene expression profilings between Bortezomib and vehicle treated cells were compared.
2017-04-10 | GSE97558 | GEO
Project description:The objective was to investigate the toxic effect of hydroxyl-modified Graphene quantum dots (GQD) on normal human esophageal epithelial cells at gene expression level. Gene expression profilings between GQD and vehicle treated cells were compared.
2017-03-17 | GSE96720 | GEO
Project description:Genome-wide analysis of the toxic effect of hydroxyl-modified Graphene quantum dots (GQD) on normal human esophageal epithelial cells
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Project description:The human miRNA profiles of esophageal squamous cell carcinoma are rarely reported. Surgically removed human ESCC tissues and matched normal esophageal epithelial tissues (5cm away from tumor) were collected to make an Agilent microarray.
2015-08-07 | GSE59973 | GEO
Project description:Esophageal squamous cell carcinoma (ESCC) is one of the most common cancers with high mortality rate. Smoking is one of the established risk factors of ESCC. However, there is limited data on molecular alterations associated with cigarette smoke exposure in esophageal cells. Understanding the effects of cigarette smoke on esophageal squamous epithelial cells at a molecular level would lead to a better understanding of the pathobiology of ESCC which has implications for identification of early biomarkers and therapeutic targets. To investigate the effect of cigarette smoke exposure, we developed a cell line model where Het1A cells (non-neoplastic human esophageal epithelial cells) were chronically treated with cigarette smoke condensate (CSC) for 2 months, 4 months, 6 months and 8 months. We carried out comparative proteomic, phosphoproteomic and whole exome sequencing analyses on CSC treated and untreated cells. Increased cell proliferation and invasion of Het1A cells was observed after chronic exposure to cigarette smoke. Using quantitative proteomic and phosphoproteomic analyses, we identified 56 proteins and 296 phosphoproteins that showed differential expression. Bioinformatics analysis of differentially expressed proteins and phosphoproteins showed enrichment of molecules involved in DNA damage response pathway. Whole exome sequencing (WES) of CSC treated and untreated cells also revealed mutations and copy number alterations in genes associated with DNA damage response. By correlating WES, proteomic and phosphoproteomic results, we observed potential loss of function in HMGN2 and MED1 that were reported as potential tumor suppressors and are known to play important role in DNA damage response. We also observed decreased expression of HMGN2 in tissue section of ESCC. Overexpression of HMGN2 and MED1 lead to decreased proliferative and invasive ability of CSC treated cells. These findings suggest that cigarette smoke affects genes and proteins associated with DNA damage response pathways which might play a vital role in development of ESCC.
2021-09-07 | PXD007799 | Pride
Project description:Esophageal squamous cell carcinoma (ESCC) is one of the most common cancers with high mortality rate. Smoking is one of the established risk factors of ESCC. However, there is limited data on molecular alterations associated with cigarette smoke exposure in esophageal cells. Understanding the effects of cigarette smoke on esophageal squamous epithelial cells at a molecular level would lead to a better understanding of the pathobiology of ESCC which has implications for identification of early biomarkers and therapeutic targets. To investigate the effect of cigarette smoke exposure, we developed a cell line model where Het1A cells (non-neoplastic human esophageal epithelial cells) were chronically treated with cigarette smoke condensate (CSC) for 2 months, 4 months, 6 months and 8 months. We carried out comparative proteomic, phosphoproteomic and whole exome sequencing analyses on CSC treated and untreated cells. Increased cell proliferation and invasion of Het1A cells was observed after chronic exposure to cigarette smoke. Using quantitative proteomic and phosphoproteomic analyses, we identified 56 proteins and 296 phosphoproteins that showed differential expression. Bioinformatics analysis of differentially expressed proteins and phosphoproteins showed enrichment of molecules involved in DNA damage response pathway. Whole exome sequencing (WES) of CSC treated and untreated cells also revealed mutations and copy number alterations in genes associated with DNA damage response. By correlating WES, proteomic and phosphoproteomic results, we observed potential loss of function in HMGN2 and MED1 that were reported as potential tumor suppressors and are known to play important role in DNA damage response. We also observed decreased expression of HMGN2 in tissue section of ESCC. Overexpression of HMGN2 and MED1 lead to decreased proliferative and invasive ability of CSC treated cells. These findings suggest that cigarette smoke affects genes and proteins associated with DNA damage response pathways which might play a vital role in development of ESCC.
2021-09-07 | PXD007814 | Pride
Project description:The current study is focused on elucidating the effect of acute alcohol challenge on esophageal epithelial cells. We employed in vivo mouse models, ex-vivo 3D-organoids and 2D cell culture to answer this question. RNA-Seq was employed to identify acute alcohol-induced transcriptional changes in human esophageal epithelial cells in-vitro. Acute-alcohol promoted strong mitochondrial damage resulting in bioenergenitic imbalance in esophageal epithelial cells. Autophagy was activated potentially via the AMPK-mTORC1 pathway to promtoe the clearance of damaged mitochondria.
2020-10-01 | GSE143479 | GEO
Project description:The human miRNA profiles of esophageal squamous cell carcinoma are rarely reported. Surgically removed human ESCC tissues and matched normal esophageal epithelial tissues (5cm away from tumor) were collected to make an Agilent microarray. Three paired of human ESCC tissues and normal controls were collected. All patients have no radiotherapy or chemotherapy before surgery. None of these three patients have distant metastasis.
2015-08-07 | E-GEOD-59973 | biostudies-arrayexpress
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.
2014-09-20 | E-GEOD-61587 | biostudies-arrayexpress
Project description:Human esophageal cancer is the sixth leading cause of cancer death worldwide. More than 90% of esophageal cancer is esophageal squamous cell carcinoma (ESCC). However, the etiological cause of ESCC remains unclear. By using gene expression microarray analysis, we aimed to find whether fungal infection is involved in ESCC development. We identified a wide spectrum of molecular signatures in a fungal infection and ESCC mouse model, including alterations involved in epigenetic regulation, cell cycle control, cell proliferation and survival signaling, and inflammation, which share many similarities with human ESCC.
2017-04-01 | GSE80005 | GEO