%0 Journal Article
%T Knockdown of  PLAT  enhances the anticancer effect of gefitinib in non-small cell lung cancer
%A Chunxue Bai
%A Ge Zhang
%A Huayin Li
%A Jian Zhou
%A Jing Li
%A Meijia Chang
%A Mengnan Yan
%A Wei Wang
%A Wenjun Peng
%J SCIE-indexed Journal
%D 2020
%R 10.21037/jtd.2019.12.106
%X Lung cancer is the leading cause of cancer incidence and mortality worldwide, with 1.8 million people diagnosed and 1.6 million deaths due to the disease annually (1). Non-small cell lung cancer (NSCLC) accounts for nearly 85% of all cases of lung cancer (2,3). Epidermal growth factor receptor (EGFR), an extensively studied protein that promotes tumor proliferation, angiogenesis, metastatic potential, and chemo-resistance and inhibits cell apoptosis, is highly expressed on the surface of NSCLC cells and commonly mutated (4,5). Nearly 90% of EFGR mutations in NSCLC patients are attributed to the deletion of exon 19 and the L858R substitution in exon 21 (6-8). Thus, tyrosine kinase inhibitors (TKIs) targeting EGFR, such as gefitinib and erlotinib, have become an efficient first-line anti-tumor approach for such patients. However, patients receiving TKI therapy inevitably develop resistance to these drugs after about 10¨C14 months. Mechanisms of resistance include additional EGFR mutations (T790M or Cys797Ser), c-MET amplification, human epidermal growth factor receptor 2 (HER2) amplification, epithelial-mesenchymal transition (EMT), small cell lung cancer transformation, or AXL activation (7-11). Meanwhile, other mechanisms of resistance remain to be discovered
%U http://jtd.amegroups.com/article/view/35704/html