Time course of TGFbeta induced epithelial mesenchymal transition (EMT) in H358 NSCLC cells.

The capacity of cancer cells to undergo epithelial mesenchymal trans-differentiation has been implicated as a factor driving metastasis, through the acquisition of enhanced migratory/invasive cell programs and the engagement of anti-apoptotic mechanisms promoting drug and radiation resistance. Our aim was to define molecular signaling changes associated with mesenchymal trans-differentiation in two KRas mutant NSCLC models. We focused on central transcription and epigenetic regulators predicted to be important for mesenchymal cell survival. Overall design: RNA was harvested 0, 1, 2, 4, 6, 8, 18, 24, 72, 168, ~500 and ~4500 hours after TGFbeta addition and subjected to 50bp paired-end Illumina RNAseq analysis. Haley, J.A., Haughney, E., Ullman, E., Bean, J., Haley, J.D.* and Fink, M.Y. (2014) 'Altered Transcriptional Control Networks with Trans-Differentiation of Isogenic Mutant KRas NSCLC Models' Front. Oncology, doi/10.3389/fonc.2014.00344.

癌细胞发生上皮间质转分化（epithelial mesenchymal trans-differentiation）的能力，通过获得增强的迁移/侵袭细胞程序，并激活可促进药物与放射抵抗的抗凋亡机制，被认为是驱动肿瘤转移的关键诱因之一。
本研究旨在明确两种KRas突变型非小细胞肺癌（non-small cell lung cancer, NSCLC）模型中，与间质转分化相关的分子信号变化。我们聚焦于经预测对间质细胞存活至关重要的核心转录调控因子与表观遗传调控因子。
实验整体设计：在添加转化生长因子β（transforming growth factor beta, TGFβ）后的0、1、2、4、6、8、18、24、72、168、约500以及约4500小时收集RNA样本，随后对样本开展50bp双端Illumina RNA测序（RNAseq）分析。
Haley, J.A.、Haughney, E.、Ullman, E.、Bean, J.、Haley, J.D.* 与 Fink, M.Y. (2014)《同基因KRas突变非小细胞肺癌模型转分化过程中的转录调控网络改变》，《前沿肿瘤学》(Front. Oncology)，DOI: 10.3389/fonc.2014.00344。