curcumin induces egfr degradation in lung adenocarcinoma and modulates p38 activation in intestine the versatile adjuvant for gefitinib therapy姜黄素诱导表皮生长因子受体退化在肺腺癌和调节p38激活肠的多功能辅助吉非替尼治疗.pdfVIP

Curcumin Induces EGFR Degradation in Lung Adenocarcinoma and Modulates p38 Activation in Intestine: The Versatile Adjuvant for Gefitinib Therapy 1,2 1,2 3,4 5 1,2 Jen-Yi Lee , Yee-Ming Lee , Gee-Chen Chang , Sung-Liang Yu , Wan-Yu Hsieh , Jeremy J. W. 4 2 6 Chen , Huei-Wen Chen *, Pan-Chyr Yang 1 Department and Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan, 2 Graduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan, 3 Division of Chest Medicine, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan, 4 Institute of Biomedical Science, College of Life Sciences, National Chung-Hsing University, Taichung, Taiwan, 5 Department of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei, Taiwan, 6 Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University Medical College, Taipei, Taiwan Abstract Background: Non-small cell lung cancer (NSCLC) patients with L858R or exon 19 deletion mutations in epidermal growth factor receptor (EGFR) have good responses to the tyrosine kinase inhibitor (TKI), gefitinib. However, patients with wild-type EGFR and acquired mutation in EGFR T790M are resistant to gefitinib treatment. Here, we showed that curcumin can improve the efficiency of gefitinib in the resistant NSCLC cells both in vitro and in vivo models. Methods/Principal Findings: After screening 598 herbal and natural compounds, we found curcumin could inhibit cell proliferation in different gefitinib-resistant NSCL