Project description:Serglycin proteoglycans contribute to proper storage and secretion of inflammatory mediators in hematopoietic cells. Serglycin is also expressed in cancer cells where increased expression has been linked to poor prognosis. In the present study we report that serglycin proteoglycan is absolutely required for metastasis in the MMTV-PyMT-driven mouse breast cancer model. Serglycin seems to play a role in promoting epithelial to mesenchymal transition, cancer-related inflammation and extravasation. Our results suggest that serglycin and serglycin-dependent mediators are potential drug targets to prevent metastatic disease/dissemination of cancer. 6 total breast tumor samples were analyzed. 3 of SG+/- and 3 of SG-/- tumour tissue. Raw data was normalized using the robust multi-array average (RMA) method. To identify potential serglycin-regulated mediators of metastasis, we performed a microarray expression analysis of RNA isolated from SG+/- and SG-/- breast tumor tissue. The expression analysis identified 672 genes with a significantly altered expression level, at log2 fold >±1,2. Strikingly, only six genes were up-regulated in the SG-/- PyMT+ tumor cells compared to SG+/- PyMT+ tumor cells while 666 were significantly down-regulated.
Project description:Serglycin proteoglycans contribute to proper storage and secretion of inflammatory mediators in hematopoietic cells. Serglycin is also expressed in cancer cells where increased expression has been linked to poor prognosis. In the present study we report that serglycin proteoglycan is absolutely required for metastasis in the MMTV-PyMT-driven mouse breast cancer model. Serglycin seems to play a role in promoting epithelial to mesenchymal transition, cancer-related inflammation and extravasation. Our results suggest that serglycin and serglycin-dependent mediators are potential drug targets to prevent metastatic disease/dissemination of cancer.
2016-06-01 | GSE67806 | GEO
Project description:STAT3 Knock-out Breast cancer cell lines
Project description:We wished to investigate the role of E-cadherin loss in our mouse parietal cell/pre-parietal cell E-cadherin knock-out, p53 knock-out, oncogenic Kras induced model of gastric cancer. As such, we isolated RNA from stomach tissue from our E-cadherin knock-out model (Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)) and our E-cadherin heterozygous model (Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)). We then performed a microarray on this stomach tissue from four independent mice of each genotype. Differentially expressed genes were identified and gene set overlap analysis was used to identify pathways enriched in one model over the other.
Project description:Genome wide DNA methylation profiling of thymocytes from wild type and Nsd2 knock out (KO) and Nsd2 knock in (KI). The 906th Proline of Nsd2 was substituted to Leucine in Nsd2 KI by gene editing. The Illumina Infinium Mouse methylation Beadchip was used to obtain DNA methylation profiles across approximately 270,000 CpGs in thymocytes. Samples included 2 wild type, 2 heterozygous knock out, 1 heterozygous knock in, and 1 homozygous knock in.
Project description:We have analyzed the transcript expression levels in Dicer heterozygous and Dicer knock-out embryonic stem (ES) cells in order to identify which transcripts are regulated by RNAi pathway in mouse ES cells. Keywords: Cell type comparison of cell line with or without knock-out
