Project description: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.
2020-08-27 | GSE152032 | GEO
Project description:RNA-seq of neutrophils from WT and Mir4435-2hg KO mice
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.
Project description:Purpose : The goals of this study are to compare NGS-derived transcriptome profiling (RNA-seq) of colon samples of intestinal epithelial cell specific Axin1 Knockout mice and WT controls that were submitted to DSS-induced colitis and AOM/DSS-induced colorectal carcinogenesis. Methods : DSS-induced colitis was performed on Axin1flfl (WT) and Vil CreERT2;Axin1fl/fl (Axin1KOΔIEC) mice by giving 3% DSS dissolved in drinking water for 7 days and subsequently placed on regular water for recovery before sacrifice at Day 7 and D13. Methods : AOM/DSS-induced colorectal tumorigenesis was performed on Axin1flfl (WT) and Vil CreERT2;Axin1fl/fl (Axin1KOΔIEC) mice that were sacrificed at day 100 post-AOM injection to collect colorectal tumors. Methods : Colonic mRNA profiles of WT and Axin1KOΔIEC mice were generated by deep sequencing using Illumina NextSeq 500 instrument (150base-lengths read V2 chemistry in a paired-end mode)
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.
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.
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.
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.
