NDLI: Isoliquiritigenin induces apoptosis and inhibits xenograft tumor growth of human lung cancer cells by targeting both wild type and L858R/T790M mutant EGFR.

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Isoliquiritigenin induces apoptosis and inhibits xenograft tumor growth of human lung cancer cells by targeting both wild type and L858R/T790M mutant EGFR.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lee, Nam Hyouck Chi, Young-in Singh, Puja Lim, Tae-gyu Lee, Charles C. Dong, Zigang Lim, Do Young Bode, Ann M. Cho, Yong-yeon Lee, Mee-hyun Lee, Sung-young Chen, Hanyong Kim, Jong Eun Lee, Ki Won Jung, Sung Keun Jeong, Chul-ho Kundu, Joydeb Kumar
Description	Author Affiliation: Jung SK ( From The Hormel Institute, University of Minnesota, Minnesota 55912, Division of Metabolism and Functionality Research, Korea Food Research Institute, Seongnam, Gyeonggi-do, 463-746 Republic of Korea.); Lee MH ( From The Hormel Institute, University of Minnesota, Minnesota 55912, College of Pharmacy, The Catholic University of Korea, Bucheon, Gyeonggi-do, 420-743 South Korea.); Lim DY ( From The Hormel Institute, University of Minnesota, Minnesota 55912.); Kim JE ( From The Hormel Institute, University of Minnesota, Minnesota 55912, Advanced Institutes of Convergence Technology, Seoul National University, Suwon, Gyeonggi-do, 443-270 South Korea.); Singh P ( From The Hormel Institute, University of Minnesota, Minnesota 55912.); Lee SY ( From The Hormel Institute, University of Minnesota, Minnesota 55912.); Jeong CH ( From The Hormel Institute, University of Minnesota, Minnesota 55912, College of Pharmacy, Keimyung University, Daegu, 704-701 South Korea.); Lim TG ( From The Hormel Institute, University of Minnesota, Minnesota 55912, WCU Biomodulation Major, Department of Agricultural Biotechnology and Center for Food and Bioconvergence, Seoul National University, Seoul, 151-921, Republic of Korea.); Chen H ( From The Hormel Institute, University of Minnesota, Minnesota 55912.); Chi YI ( From The Hormel Institute, University of Minnesota, Minnesota 55912.); Kundu JK ( College of Pharmacy, Keimyung University, Daegu, 704-701 South Korea.); Lee NH ( Division of Metabolism and Functionality Research, Korea Food Research Institute, Seongnam, Gyeonggi-do, 463-746 Republic of Korea.); Lee CC ( From The Hormel Institute, University of Minnesota, Minnesota 55912, Department of Food Science, Cornell University, Ithaca, New York 14850, and.); Cho YY ( College of Pharmacy, The Catholic University of Korea, Bucheon, Gyeonggi-do, 420-743 South Korea.); Bode AM ( From The Hormel Institute, University of Minnesota, Minnesota 55912.); Lee KW ( Advanced Institutes of Convergence Technology, Seoul National University, Suwon, Gyeonggi-do, 443-270 South Korea, WCU Biomodulation Major, Department of Agricultural Biotechnology and Center for Food and Bioconvergence, Seoul National University, Seoul, 151-921, Republic of Korea, Research Institut); Dong Z ( From The Hormel Institute, University of Minnesota, Minnesota 55912, zgdong@hi.umn.edu.)
Abstract	Non-small-cell lung cancer (NSCLC) is associated with diverse genetic alterations including mutation of epidermal growth factor receptor (EGFR). Isoliquiritigenin (ILQ), a chalcone derivative, possesses anticancer activities. In the present study, we investigated the effects of ILQ on the growth of tyrosine kinase inhibitor (TKI)-sensitive and -resistant NSCLC cells and elucidated its underlying mechanisms. Treatment with ILQ inhibited growth and induced apoptosis in both TKI-sensitive and -resistant NSCLC cells. ILQ-induced apoptosis was associated with the cleavage of caspase-3 and poly-(ADP-ribose)-polymerase, increased expression of Bim, and reduced expression of Bcl-2. In vitro kinase assay results revealed that ILQ inhibited the catalytic activity of both wild type and double mutant (L858R/T790M) EGFR. Treatment with ILQ inhibited the anchorage-independent growth of NIH3T3 cells stably transfected with either wild type or double-mutant EGFR with or without EGF stimulation. ILQ also reduced the phosphorylation of Akt and ERK1/2 in both TKI-sensitive and -resistant NSCLC cells, and attenuated the kinase activity of Akt1 and ERK2 in vitro. ILQ directly interacted with both wild type and double-mutant EGFR in an ATP-competitive manner. A docking model study showed that ILQ formed two hydrogen bonds (Glu-762 and Met-793) with wild type EGFR and three hydrogen bonds (Lys-745, Met-793, and Asp-855) with mutant EGFR. ILQ attenuated the xenograft tumor growth of H1975 cells, which was associated with decreased expression of Ki-67 and diminished phosphorylation of Akt and ERK1/2. Taken together, ILQ suppresses NSCLC cell growth by directly targeting wild type or mutant EGFR.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	52
Volume Number	289
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2014-12-26
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antineoplastic Agents, Phytogenic Pharmacology Apoptosis Drug Effects Chalcones Lung Neoplasms Drug Therapy Receptor, Epidermal Growth Factor Genetics Animals Cell Line, Tumor Cell Proliferation Extracellular Signal-Regulated MAP Kinases Metabolism HEK293 Cells Pathology Mice Mice, Nude Mutation, Missense NIH 3T3 Cells Protein Binding Protein Processing, Post-Translational Proto-Oncogene Proteins C-akt Antagonists & Inhibitors Tumor Burden Xenograft Model Antitumor Assays Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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