Two lung cancer cell lines with EGFR mutations, PC-9 and KHM-3S, were either treated with Tarceva for 24 hours or left untreated. The gene expression profiles were examined by RNAseq, and the genome wide binding profiles of total STAT3 and pSTAT3 were characterized by ChIPseq.

Lung cancers harboring activating EGFR mutants show dramatic responses to EGFR TKIs, such as Tarceva. However, nearly all patients show relapse within 1 year after initial treatment. To investigate the early signaling switches that are involved in the formation of drug resistance, and the role of STAT3 in the early signaling switches involved in the formation of drug resistance, we have treated two lung cancer cell lines with EGFR mutations, PC-9 and KMH-3S, with Tarceva for 24hours. The RNA samples with and without treatment were collected in triplicate for RNAseq experiment.The total STAT3 and pSTAT3 chromatinIP were done on samples with and without treatment for ChIPseq.EGA study EGAS00001000793

携带激活型EGFR突变的肺癌患者对EGFR酪氨酸激酶抑制剂（EGFR TKIs，如特罗凯（Tarceva））可产生显著应答。然而，几乎所有患者在初始治疗后的1年内均会出现复发。为探究参与耐药形成的早期信号转换机制，以及STAT3在该类耐药相关早期信号转换中的作用，我们使用特罗凯（Tarceva）处理两款携带EGFR突变的肺癌细胞系PC-9与KMH-3S，处理时长为24小时。我们收集处理组与对照组的RNA样本各三份生物学重复，用于RNA测序（RNAseq）实验。同时，针对处理组与对照组样本，分别开展总STAT3与磷酸化STAT3（pSTAT3）的染色质免疫沉淀实验，所得样本用于染色质免疫沉淀测序（ChIPseq）。本研究为EGA数据库中编号为EGAS00001000793的研究项目。