Gene expression profiels from organoids.

Recent studies have suggested increased plasticity of differentiated cells within the intestine to act both as intestinal stem cells and tumour initiating cells. However, little is known of the processes that regulate this plasticity. Our previous work has shown that activating mutations of Kras or the NF-kB pathway can drive dedifferentiation of intestinal cells lacking Apc. To investigate this process further, we profiled organoids by gene expression analysis. Organoids were isolated from VillinCreER Apcfl/fl KrasG12D crypts (here called CC) or Villi (here called SFV). Two-condition experiments, CC and SFV organoids. Biological replicates: 3 CC and 3 SFV independently grown and harvested. One replicate per array. Each replicate represents a single mouse.

近期已有研究表明，肠道内分化细胞的可塑性显著增强，可同时充当肠道干细胞（intestinal stem cells）与肿瘤起始细胞（tumour initiating cells）。然而，目前对于调控该可塑性的具体分子过程仍知之甚少。我们此前的研究证实，KRAS或核因子κB（NF-κB）通路的激活性突变，可驱动缺失APC的肠道细胞发生去分化。为进一步探究该过程的具体机制，我们通过基因表达分析对类器官（organoids）进行了基因表达谱分析。本研究中的类器官分别分离自VillinCreER Apcfl/fl KrasG12D基因型小鼠的肠隐窝（crypts，以下简称CC组）及小肠绒毛（以下简称SFV组）。本实验包含两组样本：CC组类器官与SFV组类器官。生物学重复设置为：CC组与SFV组各3例，所有样本均经独立培养并收获；每个生物学重复对应一张基因芯片，且每个重复均来自1只单独的实验小鼠。