Shikonin sensitizes wild‑type EGFR NSCLC cells to erlotinib and gefitinib therapy
作者： Yang‑Ling Li , Xiu Hu , Qing‑Yu Li , Fei Wang , Bo Zhang
关键词: A549 cell 、 Gefitinib 、 Oncogene 、 Epidermal growth factor receptor 、 Cell cycle 、 Erlotinib 、 Medicine 、 Apoptosis 、 Unfolded protein response 、 Cancer research
摘要: As patients with non-small cell lung cancer (NSCLC) and wild-type epidermal growth factor receptor (EGFR) are resistant to treatment erlotinib or gefitinib, potential chemosensitizers required potentiate EGFR NSCLC cells erlotinib/gefitinib treatment. The present study reported that shikonin could sensitize the anticancer activity of in cells. Furthermore, mitochondrial-mediated apoptosis induced by In addition, demonstrated induce activating reactive oxygen species (ROS)-mediated endoplasmic reticulum (ER) stress, may also ER stress cells; however, plus was more effective than either agent alone. This indicated ROS-mediated be associated enhanced mitochondrial erlotinib/gefitinib. promote transition cytoprotective stress-inducing EGFR-tyrosine kinase inhibitor tolerance apoptosis-promoting stress. enhance anti-NSCLC vivo. data a sensitizer anti-cancer efficacy
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