Resibufogenin (RBG) is an active ingredient of
toad venom that also has antitumor potential. The present study aimed to investigate the role of RBG in
multiple myeloma (MM) and the underlying action mechanism involving the PI3K/Akt signaling pathway. A human MM cell line, RPMI8226, was treated with RBG and/or
insulin-like growth factor 1 (IGF-1; an activator of the PI3K/AKT signaling pathway). Cell viability and apoptosis were detected using Cell Counting Kit-8 and flow cytometry, respectively. Cell migration and invasion were detected using a Transwell assay. In addition, the epithelial-mesenchymal transition (EMT)-associated
proteins (
E-cadherin,
N-cadherin and
Vimentin) and the PI3K/AKT pathway-associated
proteins [AKT, phosphorylated (p)-AKT, PI3K and p-PI3K] were measured using western blotting. RBG inhibited the viability, migration and invasion, and promoted the apoptosis of RPMI8226 cells in a dose-dependent manner. RBG at concentrations of 4 and 8 µM upregulated
E-cadherin, and downregulated
N-cadherin and
Vimentin in RPMI8226 cells. RBG also decreased the
protein expression of p-AKT and p-PI3K in a dose-dependent manner. In addition, the intervention of
IGF-1 weakened the inhibitory effects of RBG on the malignant characteristics of MM cells. RBG-induced inhibition of EMT and the PI3K/AKT pathway were also weakened by
IGF-1 treatment. In conclusion, RBG inhibited viability, migration, invasion and EMT, and promoted the apoptosis of MM cells by blocking the PI3K/AKT signaling pathway.