Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Ablation of S1PR4 triggers CD8+ T cell expansion to reduce tumor growth and improve therapy

ABSTRACT: We studied the role of S1PR4 on tumor progression using the PyMT mammary carcinoma mouse model and the AOM/DSS model for colitis-associated cancer. To gain insights of the underlying mechanism how S1PR4 ablation resulted in enhanced intratumoral CD8+ T cell abundance, we performed whole transcriptome profiling of total WT and S1PR4 KO colons subjected to the AOM/DSS model (day 84) as well as FACS-sorted CD8+ T cells from WT and S1PR4 KO tumors of PyMT mice. Next-generation mRNA sequencing, in triplicates, on a NextSeq 500 (PyMT CD8+ T cells) or a HiSeq 2000 (AOM/DSS model) high-throughput sequencer was used.

ORGANISM(S): Mus musculus

PROVIDER: GSE152032 | GEO | 2020/08/27

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Dnase1l3 enhances antitumor immunity and suppresses tumor progression [bulk RNAseq]

Project description:For the chronic inflammation-related colon cancer model (AOM/DSS-colon cancer model), 3-month-old Dnase1l3 WT and KO mice were injected with AOM (8 mg/kg, body weight). One week later, mice were challenged with 2.5% DSS water for 7 days followed by a 14-day recovery with regular drinking water for three cycles. Body weight, rectal bleeding and diarrhea were monitored during the entire experiment. Mice with more than 25% weight loss were removed during the experiment. For the AOM model, 2-month-old Dnase1l3 WT and KO mice were injected intraperitoneally with AOM (8 mg/kg, body weight). Colon tissues were isolated 9 hours, or five days after injection. All animal experiments were conducted in accordance with guidelines of NIEHS/NIH Animal Care and Use Committee.

2022-02-07 | GSE196076 | GEO

Dnase1l3 enhances antitumor immunity and suppresses tumor progression [scRNAseq]

2022-02-07 | GSE196054 | GEO

mRNAs and miRNAs expression data from AOM/DSS, AOM, DSS and control mouse colon epithelial tissue at day100 when tumor formed in AOM/DSS bearing mice --- miRNA microarray

Project description:To find out which miRNAs are significantly differential expression and potentially involved in the process of inflammation promoting carcinogenesis of colorectal cancer (CRC). We established a colitis-associated CRC (AOM/DSS, Azoxymethane/Dextran sulfate sodium salt) model, colitis (DSS) model and high dose carcinogen (AOM, about 5 times AOM amount given than AOM/DSS model) model. At day 100 when tumor formed in AOM/DSS bearing mice (colitis-associated CRC mice) but no tumor was found in AOM (high dose carcinogen) and DSS model, we employed miRNA microarray as a discovery platform to identify genes with the potential to involve in the progression of CRC promoted by inflammation. 5-7 weeks female BALB/c mice, (1) AOM/DSS group: AOM 12.5mg/kg i.p. at day 1, DSS drinking 5d/21dx3circles from day 5; (2) AOM group: AOM 10mg/kg i.p. 1/weekx6 from day 1; (3) DSS group: DSS drinking 5d/21dx3circles from day 5. The distal colon epithelial tissues were collected at day100 when tumor formed in AOM/DSS bearing mice. The miRNA microarray experiments were performed together.

2013-05-10 | E-GEOD-44983 | biostudies-arrayexpress

mRNAs and miRNAs expression data from AOM/DSS, AOM, DSS and control mouse colon epithelial tissue at day100 when tumor formed in AOM/DSS bearing mice --- mRNA expression data

Project description:To find out which mRNAs are significantly differential expression and potentially involved in the process of inflammation promoting carcinogenesis of colorectal cancer (CRC). We established a colitis-associated CRC (AOM/DSS, Azoxymethane/Dextran sulfate sodium salt) model, colitis (DSS) model and high dose carcinogen (AOM, about 5 times AOM amount given than AOM/DSS model) model. At day 100 when tumor formed in AOM/DSS bearing mice (colitis-associated CRC mice) but no tumor was found in AOM (high dose carcinogen) and DSS model, we employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to involve in the progression of CRC promoted by inflammation. 5-7 weeks female BALB/c mice, (1) AOM/DSS group: AOM 12.5mg/kg i.p. at day 1, DSS drinking 5d/21dx3circles from day 5; (2) AOM group: AOM 10mg/kg i.p. 1/weekx6 from day 1; (3) DSS group: DSS drinking 5d/21dx3circles from day 5. The distal colon epithelial tissues were collected at day100 when tumor formed in AOM/DSS bearing mice. The whole genome microarray expression profiling experiments were performed together.

2013-05-10 | E-GEOD-44904 | biostudies-arrayexpress

Analysis of the role of Dectin-1 in the development of intestinal tumorigenesis [RNA-Seq]

Project description:To investigate the potential role of Dectin-1 in the development of intestinal tumorigenesis, we used Dectin-1 deficient (Clec7a–/–, KO) mice under germ-free (GF) condition and azoxymethane (AOM) and 3 cycles of dextran-sodium-sulfate (DSS)-induced mouse colorectal tumor model to compare with wild-type (WT) mice.

2023-02-21 | GSE221205 | GEO

mRNAs and miRNAs expression data from AOM/DSS, AOM, DSS and control mouse colon epithelial tissue at day100 when tumor formed in AOM/DSS bearing mice --- miRNA microarray

2013-05-10 | GSE44983 | GEO

mRNAs and miRNAs expression data from AOM/DSS, AOM, DSS and control mouse colon epithelial tissue at day100 when tumor formed in AOM/DSS bearing mice --- mRNA expression data

2013-05-10 | GSE44904 | GEO

Microarray analysis of colon tissue of DSS colitis STAP-2 KO mice

Project description:To identify STAP-2 regulating genes modulated intestine inflammation, we conducted microarray analyses using colon tissue from pooled WT (n=3) or STAP-2-/- mice (n=3) treated with DSS for 3 days. Bioinformatic analyses revealed that STAP-2 deletion mediates insufficient immune and inflammatory reaction through altering a series of associated gene expression. The DSS-treated colons derived from WT (n=3) and STAP-2 KO (n=3) mice were examined. Each strain was run in biological duplicate.

2014-04-17 | E-GEOD-48543 | biostudies-arrayexpress

Thrombospondin 1 in a model of colorectal carcinogenesis

Project description:By using a model of inflammation-induced carcinogenesis the effects of TSP-1 in induced tumors were analyzed. Mice received a single injection of azoxymethane (AOM) and multiple cycles of dextran sodium sulfate (DSS) for inducing chronic inflammation-related cancers. Proliferation and angiogenesis status were analyzed as well as their transcript profile by using a gene microarray approach. We used Affymetrix GeneChips to determine the changes in the genetic profile between WT and TSP-1 deficient tumors in a model of colorectal carcinogenesis. We identified differentially expressed genes between WT and TSP-1 deficient tumors. WT and TSP-1 deficient mice were with a single injection of AOM and were drinking 1.5%DSS (dextran sulfate sodium) to induce colitis in four cycles. Wt mice drinking water only was used as reference. Mice were sacrificed and tumors excised for these studies and morphological analyses

2015-08-26 | E-GEOD-60805 | biostudies-arrayexpress

LGR5 positivity defines stem-like cells in colorectal cancer

Project description:To further elucidate the role of the intestinal stem cell marker Leucine-rich-repeat-containing G-protein-coupled receptor 5 (LGR5) in colorectal cancer (CRC), we exposed Lgr5-EGFP-IRES-Cre-ERT2 mice to azoxymethane/dextrane sodium sulfate (AOM/DSS) which induces inflammation-driven colon tumors. Tumors were then flow-sorted into fractions of epithelial cells that expressed high or low levels of Lgr5 and were characterized using gene expression profiling. In the AOM/DSS-induced mouse colon tumors Lgr5 high cells showed higher levels of several stem cell-associated genes and higher Wnt signaling than Lgr5 low tumor cells and Lgr5 high normal colon epithelial cells. To further elucidate the role of the intestinal stem cell marker Leucine-rich-repeat-containing G-protein-coupled receptor 5 (LGR5) in colorectal cancer (CRC), we transduced SW480 CRC cells with lentiviral shRNA constructs to silence LGR5 expression. This resulted in a depletion of spheres but did not affect adherently growing cells. Spheres expressed higher levels of several stem cell-associated genes than adherent cells. Notch signaling was down-regulated upon LGR5 silencing. This was confirmed by immunohistochemistry against cleaved NOTCH1. Normal mouse colons and AOM/DSS-induced mouse colon tumors were flow-sorted into Lgr5 high and low cells before gene expression was measured. Fifteen independent experiments were performed using seven individual mice for normal colons and eight for tumors. Appropriate LGR5 status was confirmed by real-time qRT-PCR before measuring silencing induced gene expression. Three independent experiments were performed for each cell fraction using separately cultured cells for each experiment.

2013-04-19 | E-GEOD-46200 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data