→ 한국식품과학회지2018 ; 50(01): 105-110
Melittin inhibits cell migration and invasion via blocking of the epithelial-mesenchymal transition (EMT) in lung cancer cells
EMT 억제를 통한 멜리틴의 폐암세포 이동 및 침투 억제 효과
Hyun-Ji Cho1,2, Yun-Jeong Jeong1,2, Mun-Hyeon Kim1,2, Il-Kyung Chung3, Dong Wook Kang4, and Young-Chae Chang1,2,*
1Research Institute of Biomedical Engineering, 2Department of Medicine, Catholic University of Daegu School of Medicine, 3Department of Biotechnology, Catholic University of Daegu, 4Department of pharmaceutical science and technology, Catholic University of Daegu
1대구가톨릭대학교 의용생체공학연구소, 2대구가톨릭대학교 의과대학 세포생물학교실, 3대구가톨릭대학교 생명공학과, 4대구가톨릭대학교 제약산업공학과
Melittin is the main component of apitoxin (bee venom) that has been reported to have anti-inflammatory and anti-cancer effects. Herein, we demonstrated that inhibition of epithelial-mesenchymal transition (EMT) by melittin causes suppression of cancer cell migration and invasion. Melittin significantly suppressed the epidermal growth factor (EGF)-induced cell migration and invasion in lung cancer cells. Moreover, melittin up-regulated the expression of epithelial marker protein, E-cadherin, and down-regulated the expression of EMT related proteins, vimentin and fibronectin. Mechanistic studies revealed that melittin markedly suppressed the expression of EMT mediated transcription factors, ZEB2, Slug, and Snail. The EGF-induced phosphorylation of AKT, mTOR, P70S6K, and 4EBP1 was also inhibited by melittin, but not that of ERK and JNK. Therefore, the inhibitory effect of melittin on migration and invasion of lung cancer cells may be associated with the inhibition of EMT via blocking of the AKT-mTOR-P70S6K-4EBP1 pathway.
melittin, epithelial-mesenchymal transition (EMT), migration, invasion, lung cancer
한국식품과학회지 2018 Feb; 50(01): 105 - 110