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an in vivo c. elegans model system for screening egfr-inhibiting anti-cancer drugs一个体内秀丽隐杆线虫模型系统筛查egfr-inhibiting抗癌药物
An In Vivo C. elegans Model System for Screening EGFR-
Inhibiting Anti-Cancer Drugs
1 2 1 3 4 5
Young-Ki Bae , Jee Young Sung , Yong-Nyun Kim , Sunshin Kim , Kyeong Man Hong , Heung Tae Kim ,
6 6 1
Min Sung Choi , Jae Young Kwon , Jaegal Shim *
1 Comparative Biomedicine Research Branch, National Cancer Center, Ilsandong-gu, Goyang-si, Gyeonggi-do, Korea, 2 Pediatric Oncology Research Branch, National
Cancer Center, Ilsandong-gu, Goyang-si, Gyeonggi-do, Korea, 3 New Experimental Therapeutics Branch, National Cancer Center, Ilsandong-gu, Goyang-si, Gyeonggi-do,
Korea, 4 Cancer Cell and Molecular Biology Branch, National Cancer Center, Ilsandong-gu, Goyang-si, Gyeonggi-do, Korea, 5 Center for Lung Cancer, National Cancer
Center, Ilsandong-gu, Goyang-si, Gyeonggi-do, Korea, 6 Department of Biological Sciences, Sungkyunkwan University, Suwon, Gyeonggi-do, Korea
Abstract
The epidermal growth factor receptor (EGFR) is a well-established target for cancer treatment. EGFR tyrosine kinase (TK)
inhibitors, such as gefinitib and erlotinib, have been developed as anti-cancer drugs. Although non-small cell lung
carcinoma with an activating EGFR mutation, L858R, responds well to gefinitib and erlotinib, tumors with a doubly mutated
EGFR, T790M-L858R, acquire resistance to these drugs. The C. elegans EGFR homolog LET-23 and its downstream signaling
pathway have been studied extensively to provide insight into regulatory mechanisms conserved from C. elegans to
humans. To develop an in vivo screening system for potential cancer drugs targeting specific EGFR mutants, we expressed
three LET-23 chimeras in which the TK domai
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