Unknown,Transcriptomics,Genomics,Proteomics

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The differences between CD166+ pancreatic cancer cells and CD166- cells

ABSTRACT: Microarray analyses using CD166+ and CD166- pancreatic cancer cell lines from both Panc-1 and SW1990 cells. We carried out microarray analyses using the CD166+ and CD166- separated cells from both Panc-1 and SW1990. The quality of the RNA samples was evaluated using a 2100 Bioanalyzer (Agilent Technologies, Waldbronn, Germany). We used a Human HT-12v4 Expression BeadChip (Illumina, San Diego, CA) for these analyses. The data were analyzed using BeadStudio software version 3.2.3 (Illumina).

ORGANISM(S): Homo sapiens

SUBMITTER: Kenji Fujiwara

PROVIDER: E-GEOD-55294 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Dendritic cells (DC) play a vital role in the induction of activation or tolerance of immune response. STAT3 is a master transcriptional regulator of immune response in DCs by positively or negatively regulating DC function, but the mechanisms are unknown. STAT3 is post-translationally modified by acetylation or phosphorylation. While much is understood about transcriptional targets of phosphorylated STAT3, the gene targets and the functional impact of acetylated-STAT3 remain unclear. We aimed to answer the gene targets of acetylated-STAT3 and test the hypothesis that acetylation of STAT3 plays a key role in negative regulation of DCs. We performed genome-wide binding analysis of acetyl-STAT3 by ChIP-Seq coupled with gene expression microarrays. Acetylation of STAT3 induced by SAHA increased its capability to bind to target DNA sites in genome. Theses binding sites were mostly proximal but some were also distal up to over 100 kb from transcription start site. Gene expression array showed 1701 genes up-regulated and 1668 genes down-regulated. Proximal binding of acety-STAT3 showed more effective transcription function than distal binding. In top 500 binding peaks, the frequency of canonical motifs bound by acetyl-STAT3 were significantly higher than that for noncanonical motifs (p<0.00001). Functional analysis revealed that acetyl-STAT3 regulates target genes by upregulating genes that are primarily involved in negative regulation of cytokine production and IL-10 signaling, or downregulating genes that are primarily involved in immune effector process and antigen processing/presentation. Upregulation of IL-10Ra by acetyl-STAT3 contributes to the enhanced sensitivity of IL-10 signaling and negative regulation of DC function. Bone marrow derived dendritic cells were treated with SAHA (500 nm) or diluent for 12 hours. ChIP was performed using antibodies against STAT3, H3K4me3 and matched IgG control. DNA binding profiles were generated by deep sequencing using Illumina HiSeq 2000.

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The differences between CD166+ pancreatic cancer cells and CD166- cells

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