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Transcriptome analysis of HGC-27 after infection with Sendai virus

ABSTRACT: To better understand the interactions between Hippo signaling and antiviral signaling at transcription level, a high-throughput RNA-seq technology was utilized in gastric cancer cells HGC-27 at 48 hours after Sendai virus (SeV) infection.

ORGANISM(S): Homo sapiens

PROVIDER: GSE107096 | GEO | 2018/01/09

SECONDARY ACCESSION(S): PRJNA418982

REPOSITORIES: GEO

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Transcriptome analysis of HGC-27 after infection with Sendai virus

Project description:Transcriptome analysis of HGC-27 after infection with Sendai virus

| PRJNA418982 | ENA

Whole transcriptomes analyses of gastric cancer HGC-27 cell line treated with SHAP or control peptide

Project description:Purpose: To explore the molecular mechanisms of SHAP peptide (also termed as SOS) regulating gastic cancer tumorigenesis, RNA sequencing was performed to analyze the geome-wide change of SHAP treated HGC-27 cells compared to those of control peptide cells. Methods: Total mRNA was extracted from HGC-27 cells. Then RNA quality was assessed using an Agilent Bioanalyzer 2100 and the sample reads were sequenced using Illumina Hiseq 4000 platform. As a reasult, we got the transcript data using Hisat2 followed by Stringtie. qRT–PCR validation was performed using TaqMan and SYBR Green assays. Results: We mapped about 60 million sequence reads per sample to the human genome and identified about 58,000 transcripts in HGC-27 cells. Apprioximately 1,000 transcripts showed different expression between siSTRN3 and n.c. HGC-27 cells, with a fold change ≥2 and p value <0.05. Gene set enrichment analysis (GSEA) showed a significantly negative enrichment of Hippo target genes. Conclusion: Our study present the datiled transcripts analysis of HGC-27 cells, with biologic replicates. Based on RNA-seq transcriptome characterization , we conclude a molecular mechanism of SHAP regulating Hippo pathway in gastric cancer.

2020-06-05 | GSE135086 | GEO

Whole transcriptomes analyses of gastric cancer HGC-27 cell line treated with siSTRN3 mixture or negative control siRNA

Project description:Purpose: To explore the molecular mechanisms of STRN3 regulating gastic cancer tumorigenesis, RNA sequencing was performed to analyze the geome-wide change of siSTRN3 treated HGC-27 cells compared to those of control cells. Methods: Total mRNA was extracted from HGC-27 cells in triplicate respectively. Then RNA quality was assessed using an Agilent Bioanalyzer 2100 and the sample reads were sequenced using Illumina Hiseq 4000 platform. As a reasult, we got the transcript data using Hisat2 followed by Stringtie. qRT–PCR validation was performed using TaqMan and SYBR Green assays. Results: We mapped about 60 million sequence reads per sample to the human genome and identified about 58,000 transcripts in HGC-27 cells. Apprioximately 1,000 transcripts showed different expression between siSTRN3 and n.c. HGC-27 cells, with a fold change ≥2 and p value <0.05. Gene set enrichment analysis (GSEA) showed a significantly negative enrichment of Hippo target genes. Conclusion: Our study present the datiled transcripts analysis of HGC-27 cells, with biologic replicates. Based on RNA-seq transcriptome characterization , we conclude a molecular mechanism of STRN3 regulating Hippo pathway in gastric cancer.

2020-06-05 | GSE135085 | GEO

HGC-RACK1

Project description:MicroRNA microarray profiling analysis was performed on human gastric cancer HGC cells after RACK1 silenced or not

2016-03-01 | E-MTAB-3484 | biostudies-arrayexpress

Gene expression profile of sendai virus infected primary MEFs.

Project description:To investivate the role of mitochondrial-mediate antiviral innate immunity in MEFs, we performed Sendai virus (SeV) infection experiments at the different cultured conditions of the cells. We analyzed the gene expression profile of MEFs that infected or uninfected with SeV either cultured the cells under glucose or galactose medium, and investigate its differences. We found that the both cultured conditions of cells showed normal antiviral responses.

2017-05-31 | GSE75399 | GEO

Airway Epithelial Cell Response to Sendai virus infection

Project description:Oligonucleotide microarrays were used to establish a profile for gene expression in wild-type airway epithelial cells after paramyxoviral infection. Analysis was performed on mRNA isolated from SeV-infected primary-culture mouse tracheal epithelial cells that were maintained under physiologic conditions (air-liquid interface). Experiment Overall Design: Primary-culture mouse tracheal epithelial cells (mTECs) were established on Transwell membranes using air-liquid interface (ALI) conditions. Sendai virus (SeV), strain 52, was obtained from American Type Culture Collection and stored at -70Â°C. Cultures were inoculated with SeV or an equivalent amount of UV-inactivated SeV (SeV-UV) in the apical compartment for 1 h at 37 Â°C. Air-liquid-interface conditions were re-established by washing the membrane with PBS. Each culture well was subjected to one of two treatments (SeV, or UV-SeV) for 1 day. N = 4 SeV wells, N = 6 UV-SeV wells, with each well independently analyzed by microarray. No technical replicates were performed, but arrays were evaluated for quality control using the SimpleAffy package (Miller CJ, 2004) in Bioconductor 2.0.

2009-04-25 | E-GEOD-10211 | biostudies-arrayexpress

Macrophage Response to Sendai virus infection.

2005-10-10 | GSE2935 | GEO

Transcription profiling of mouse macrophage response to sendai virus infection.

Project description:Thus, mouse macrophage cultures were established from PBMCs isolated from wild-type control mice and were inoculated with SeV (Sendai virus) or UV-SeV (UV-inactivated SeV). These microarrays were performed in concert with assays of CCL5 and CCR5 expression, viral replication, and cellular apoptosis. Initial experiments indicated that wild-type mouse macrophages inoculated with SeV exhibit induction of CCL5 mRNA to the highest level of any known mouse gene product, while mRNA levels for CCL5 receptors (CCR5 as well as CCR3 and CCR1) or alternative ligands for these receptors (CCL3 and CCL4) were relatively unchanged by viral infection. Experiment Overall Design: Macrophages were pooled from mice and subsequently cultured (~3 mice/well). Each culture well was then subjected to one of two treatments (SeV, or UV-SeV) for 4 days. Thus, per condition, N = 2 culture wells, with each well independently analyzed by microarray. No technical replicates were performed, but arrays were evaluated for quality control using the SimpleAffy package (Miller CJ, 2004) in Bioconductor 1.5.

2008-06-12 | E-GEOD-2935 | biostudies-arrayexpress

Viral and transgene-free human induced pluripotent stem (iPS) cells using non-integrating Sendai virus (SeV) vectors.

Project description:Whole-genome expression analysis of non-integrating Sendai virus (SeV) vector and retroviral vector-generated human iPS cells. Parental fibroblast and induced pluripotent stem (iPS) cells.

2010-09-22 | E-GEOD-24240 | biostudies-arrayexpress

Small RNA profiling during Sendai virus infection

Project description:Small RNAs were profiled during Sendai virus infection of human A549 cells to identify changes in microRNA abundance during the cellular antiviral response. Examination of microRNA abundance during Sendai virus infection.

2013-06-10 | E-GEOD-43966 | biostudies-arrayexpress

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