NCBI Logo
GEO Logo
   NCBI > GEO > Accession DisplayHelp Not logged in | LoginHelp
GEO help: Mouse over screen elements for information.
          Go
Series GSE56468 Query DataSets for GSE56468
Status Public on Apr 03, 2014
Title Pten null prostate epithelium promotes localized myeloid-derived suppressor cell expansion and immune suppression during tumor initiation and progression [cell lines]
Organism Mus musculus
Experiment type Expression profiling by array
Summary Chronic inflammation is known to associate with prostate cancer development, but how epithelium-associated cancer initiating events cross-talk to inflammatory cells during prostate cancer initiation and progression is largely unknown. Using the Pten null murine prostate cancer model, we show an expansion of Gr-1+CD11b+ myeloid-derived suppressor cells (MDSCs) occurring intra-prostatically immediately following epithelium-specific Pten deletion without expansion in hematopoietic tissues. This MDSC expansion is accompanied by sustained immune suppression. Prostatic Gr-1+CD11b+ cells, but not those isolated from the spleen of the same tumor bearing mice, suppress T cell proliferation and express high levels of Arginase 1 and iNOS. Mechanistically, loss of PTEN in the epithelium leads to a significant upregulation of genes within the inflammatory response and cytokine-cytokine receptor interaction pathways, including Csf-1 and IL-1β, two genes known to induce MDSC expansion and immunosuppressive activities. Treating Pten null mice with the selective CSF-1 receptor inhibitor GW2580 decreases MDSC infiltration and relieves the associated immunosuppressive phenotype. Our study indicates that epithelium-associated tumor initiating events trigger the secretion of inflammatory cytokines and promote localized MDSC expansion and immune suppression, thereby promoting tumor progression
 
Overall design Custom Agilent 4x44K whole mouse genome expression oligonucleotide microarrays were used to measure transcript levels in murine Pten null prostate cancer cell lines. Benign mouse prostate epithelia as wild type control against cell lines. Each cohort had three biological replicates.
 
Contributor(s) Garcia AJ, Ruscetti M, Arenzana TL, Tran LM, Bianchi-Frias D, Sybert E, Priceman SJ, Wu L, Nelson PS, Smale ST, Wu H
Citation(s) 24662052
Submission date Apr 02, 2014
Last update date Sep 09, 2014
Contact name Linh My Tran
E-mail(s) linhtran@ucla.edu
Organization name University of Los Angeles
Department Medicine - Pulmonary & Critical Care
Lab Dubinett Lab
Street address Box 951690, 37-131 CHS
City Los Angeles
State/province California
ZIP/Postal code 90095-1690
Country USA
 
Platforms (1)
GPL10361 Agilent-016579 Nelson Whole Mouse Genome Microarray 4x44K
Samples (15)
GSM1361953 Benign Prostate Epithelial Cell Replicate 1
GSM1361954 Benign Prostate Epithelial Cell Replicate 2
GSM1361955 Benign Prostate Epithelial Cell Replicate 3
This SubSeries is part of SuperSeries:
GSE56470 Pten null prostate epithelium promotes localized myeloid-derived suppressor cell expansion and immune suppression during tumor initiation and progression
Relations
BioProject PRJNA243378

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE56468_RAW.tar 231.3 Mb (http)(custom) TAR (of TXT)
Processed data included within Sample table

| NLM | NIH | GEO Help | Disclaimer | Accessibility |
NCBI Home NCBI Search NCBI SiteMap