miR-26a desensitizes non-small cell lung cancer cells to tyrosine kinase inhibitors by targeting PTPN13

摘要: // Shudi Xu 1, 2, * , Tao Wang 3, Zhiwei Yang 4, Ying Li 5, Weijie 6 Ting 7 Shan Lintao Jia Shengli Zhang 4 Shengqing 1 Department of Respiratory Medicine, Huashan Hospital, Fudan University, Shanghai, China 2 9th Hospital Xi’an, 3 Neurology, Shaanxi Provincial People's Xi'an, Applied Physics, Xi’an Jiaotong 5 Second Biochemistry and Molecular Biology, Fourth Military Medical These authors have contributed equally to this work Correspondence to: Li, email: shengqingli@hotmail.com Zhang, zhangsl@mail.xjtu.edu.cn Keywords: epidermal growth factor receptor, tyrosine kinase inhibitor, non-small cell lung cancer, miR-26a, protein phosphatase non-receptor type 13 Received: February 16, 2016      Accepted: May 23, Published: June 07, 2016 ABSTRACT Epidermal receptor (EGFR)-targeted inhibitors (TKIs) emerged as first-line drugs for cancers (NSCLCs). However, the resistance TKIs represents key limitation their therapeutic efficacy. We found that miR-26a was upregulated in gefitinib-refractory NSCLCs; is downstream EGFR signaling directly targets silences (PTPN13) maintain activation Src, a dephosphorylation substrate PTPN13, thus reinforcing pathway regulatory circuit. inhibition significantly improved NSCLC responses gefitinib. data revealed novel mechanism TKI treatment.