TY - JOUR
T1 - Melittin inhibits cell migration and invasion via blocking of the epithelial-mesenchymal transition (EMT) in lung cancer cells
AU - Cho, Hyun Ji
AU - Jeong, Yun Jeong
AU - Kim, Mun Hyeon
AU - Chung, Il Kyung
AU - Kang, Dong Wook
AU - Chang, Young Chae
N1 - Publisher Copyright:
© The Korean Society of Food Science and Technology.
PY - 2018/2
Y1 - 2018/2
N2 - 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.
AB - 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.
KW - Epithelial-mesenchymal transition (EMT)
KW - Invasion
KW - Lung cancer
KW - Melittin
KW - Migration
UR - https://www.scopus.com/pages/publications/85046284812
U2 - 10.9721/KJFST.2018.50.1.105
DO - 10.9721/KJFST.2018.50.1.105
M3 - Article
AN - SCOPUS:85046284812
SN - 0367-6293
VL - 50
SP - 105
EP - 110
JO - Korean Journal of Food Science and Technology
JF - Korean Journal of Food Science and Technology
IS - 1
ER -
