Bee venom of Apis mellifera is a
traditional medicine in Asia. It has been used with promoting results for the treatment of
pain, rheumatoid, and
cancer disease. The purpose of this study was to investigate the effects of
bee venom on
epidermal growth factor (
EGF)-induced epithelial-mesenchymal transition (EMT) in
non-small cell lung cancer (NSCLC) and determine possible signaling pathway affected in
EGF-induced EMT in A549 cells.
Bee venom inhibited
EGF-induced
F-actin reorganization and cell invasion, and suppressed
EGF-induced EMT, processes associated with
tumor metastasis in NSCLC.
Bee venom enhanced the upregulation of
E-cadherin and the downregulation of
vimentin and inhibited
EGF-induced ERK, JNK, FAK, and mTOR phosphorylation in A549 cells. However, the inhibition of JNK phosphorylation by
bee venom was not related to the inhibitory effects of EMT. Furthermore, we found that
bee venom suppressed the EMT-related
transcription factors ZEB2 and Slug by blocking
EGF-induced ERK, FAK and mTOR phosphorylation.
Bee venom inhibits
EGF-induced EMT by blocking the phosphorylation of ERK, FAK, and mTOR, resulting in the suppression of ZEB2 and Slug. These data suggest
bee venom as a potential antimetastatic agent for NSCLC.