Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP) mouse stomach vs. Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP) mouse stomach microarray

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.本研究旨在探究E-钙粘蛋白（E-cadherin）缺失在我们所构建的小鼠壁细胞/前壁细胞特异性E-钙粘蛋白敲除、p53敲除联合致癌性Kras诱导的胃癌模型中的作用。为此，我们分别从两种基因型模型的胃组织中提取RNA：其一为纯合E-钙粘蛋白敲除模型（Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)），其二为E-钙粘蛋白杂合敲除模型（Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)）。随后，我们对每种基因型的四只独立实验小鼠的胃组织样本进行了基因芯片（microarray）检测。通过鉴定差异表达基因（differentially expressed genes），并运用基因集重叠分析（gene set overlap analysis），我们成功识别出相较于另一模型，在其中一种模型中显著富集的信号通路。