Gene expression profile analysis for the Fascin knockdown esophageal squamous carcinoma cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE11373 | GEO | 2008/05/08
SECONDARY ACCESSION(S): PRJNA106599
REPOSITORIES: GEO
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Project description:Fascin, an actin-binding protein, is upregulated in a variety of cancers, including esophageal squamous cell carcinoma (ESCC) and is proposed to function in cellular growth, mobility and invasiveness. Nonetheless, the molecular mechanisms through which fascin expression contributes to the proliferation and invasiveness of ESCC are unknown. To address this issue and to identify genes and biological pathways associated with fascin expression, a genome-wide gene expression analysis was performed on a fascin RNAi-depleted cell line and a corresponding ESCC cell line previously determined to express high levels of fascin. Experiment Overall Design: We used cDNA microarrays to identify genes that were differentially expressed upon fascin knockdown. For this purpose, we selected PSF8 (Fascin siRNA-depleted cell) and PSC(blank vector control cell ), two ESCC cell lines recently established in our laboratory. Total RNA from PSF8 cells and PSC cells was prepared for use with Affymetrix U133 cDNA microarrays.
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Project description:Fascin-1 mediated actin-bundling activity is central to the generation of plasma membrane protrusions required for cell migration. Dysregulation of cellular protrusions is observed in metastatic cancers, where they are required for increased invasiveness, and this is often correlated with overexpression of Fascin-1. Therefore, there is interest in generating therapeutic Fascin-1 inhibitors. We present the identification of Nb 3E11, a nanobody inhibitor of Fascin-1 actin-bundling activity, filopodia formation and cell migration. The crystal structure of the Fascin-1/Nb 3E11 complex reveals the structural mechanism of inhibition. Nb 3E11 occludes an actin-binding site on the third -trefoil domain of Fascin-1 that is currently untargeted by chemical inhibitors and induces a conformational change in the adjacent domains to stabilise Fascin-1 in an inhibitory state similar to that adopted in the presence of small molecule inhibitors. Nb 3E11 can be utilised as a tool inhibitor molecule to aid in the development of Fascin-1 targeted therapeutics.
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Project description:A novel alternative splicing isoform of LOXL2 â³e13 was expressed ubiquitously in all cell lines and ESCC tissues. In contrast to the impaired deamination enzymatic activity compared with full length LOXL2, LOXL2 â³e13 showed an enhanced ability to promote cell mobility and invasiveness in ESCC cells than full length LOXL2 through a different mechanism. We used cDNA microarrays to identify genes that were differentially expressed upon LOXL2 â³ e13 overexpressed. For this purpose, we selected LOXL2 â³ e13, WT and empty vector control transfeced ESCC KYSE150 cell lines. Total RNA was extracted,compare the gene expression patterns between LOXL2 â³e13, LOXL2 WT and empty vector control transfected cells through the Genechip Primeview Human Gene Expression Array.
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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.
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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.
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