Nsd3-Short Represses E-Cadherin Expression In A549 Lung Epithelial Cancer Cells

<strong>SGC Open Notebook Project to Characterize the HMTase NSD3</strong> <strong>Exp024 Objective: </strong>In a previous experiment (exp023), we show that siRNA-mediated knockdown of NSD3 increases expression of E-cadherin, a marker of epithelial cell identity. To determine which isoform of NSD3 is involved in promoting epithelial to mesenchymal transition, I have designed siRNA that targets either the long or short isoform and again use E-cadherin expression as a marker. Additionally, I have started using A549 lung epithelial cancer cells (https://www.atcc.org/Products/All/CCL-185) as my primary model. This cell line proliferates faster and is more amenable to <em>in vitro</em> experimentation than the H1299 cell line I was using previously.**SGC开放笔记本项目：表征组蛋白甲基转移酶（HMTase）NSD3** **实验024 研究目标：** 在前期实验（实验023）中，我们证实通过小干扰RNA（siRNA）介导的NSD3基因敲低，可上调上皮细胞身份标志物E-钙粘蛋白（E-cadherin）的表达。为明确NSD3的哪种亚型参与调控上皮间质转化（epithelial to mesenchymal transition），我设计了分别靶向其长、短两种亚型的小干扰RNA，并再次以E-钙粘蛋白的表达作为检测标志物。此外，我已选用A549肺上皮癌细胞系（https://www.atcc.org/Products/All/CCL-185）作为核心实验模型。相较于此前使用的H1299细胞系，该细胞系增殖速率更快，更适于体外（in vitro）实验操作。