Long non-coding RNA UCA1 induces non-T790M acquired resistance to EGFR-TKIs by activating the AKT/mTOR pathway in EGFR -mutant non-small cell lung cancer

摘要: // Ningning Cheng 1,* , Weijing Cai Shengxiang Ren 1 Xuefei Li 2 Qi Wang Hui Pan Mingchuan Zhao Jiayu Yishi Zhang Chao Xiaoxia Chen Ke Fei 3 Caicun Zhou and Fred R. Hirsch 4 Department of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University, University School Cancer Institute, Shanghai, P. China Lung Immunology, Thoracic Surgery, Pathology, Colorado Center, Aurora, Colorado, USA * These authors have contributed equally to this work Correspondence to: Zhou, email: Keywords : UCA1, EGFR-TKIs, acquired resistance, non-small cell lung cancer Received February 09, 2015 Accepted June 01, Published 08, Abstract The aim study was explore the role long non-coding RNA UCA1 (urothelial cancer-associated 1) in resistance epidermal growth factor receptor tyrosine kinase inhibitors ( EGFR -TKIs) -mutant (NSCLC). In our study, expression significantly increased cells patients with -TKIs. Over-expression associated a shorter progression-free survival (PFS) [13.0 vs . 8.5 months, P < 0.01] tumors respond significant relationship not observed T790M mutation (10.5 12.0 = 0.778), but non-T790M (19.0 vs. 9.0 0.023). knockdown restored gefitinib sensitivity resistant inhibited activation AKT/mTOR pathway epithelial-mesenchymal transition (EMT). mTOR inhibitor effective -expressing PC9/R. Inhibiting could change although there no difference. conclusion, influence over-expression on PFS for -TKIs from subgroup mutation. may induce by activating EMT.