Research Papers:
Inhibition of non-small cell lung cancer (NSCLC) growth by a novel small molecular inhibitor of EGFR
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Abstract
Jinsong Li1,2,3,*, Huayun Deng2,*, Meichun Hu2,*, Yuanzhang Fang2, Amanda Vaughn4, Xiaopan Cai1, Leqin Xu1, Wei Wan1, Zhenxi Li1, Shijie Chen3, Xinghai Yang1, Song Wu3, Jianru Xiao1
1Department of Orthopedic Oncology, Changzheng Hospital, The Second Military Medical University, Shanghai 200003, China
2The Institute of Biomedical Sciences, East China Normal University, Shanghai 200241, China
3Department of Orthopaedics, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, China
4Department of Molecular Biosciences, Institute of Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX 78712, USA
*These authors have contributed equally to this work
Correspondence to:
Jianru Xiao, e-mail: [email protected]
Song Wu, e-mail: [email protected]
Xinghai Yang, e-mail: [email protected]
Shijie Chen, e-mail: [email protected]
Keywords: EGFR, TKIs, NSCLC, Tumor growth
Received: October 12, 2014 Accepted: January 16, 2015 Published: February 05, 2015
ABSTRACT
The epidermal growth factor receptor (EGFR) is a therapeutic target (oncotarget) in NSCLC. Using in vitro EGFR kinase activity system, we identified a novel small molecule, WB-308, as an inhibitor of EGFR. WB-308 decreased NSCLC cell proliferation and colony formation, by causing G2/M arrest and apoptosis. Furthermore, WB-308 inhibited the engraft tumor growths in two animal models in vivo (lung orthotopic transplantation model and patient-derived engraft mouse model). WB-308 impaired the phosphorylation of EGFR, AKT, and ERK1/2 protein. WB-308 was less cytotoxic than Gefitinib. Our study suggests that WB-308 is a novel EGFR-TKI and may be considered to substitute for Gefitinib in clinical therapy for NSCLC.
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