Cantharidin inhibits melanoma cell proliferation via the miR‑21‑mediated PTEN pathway

Cantharidin (CTD) is an active component isolated from the blister beetle that has been demonstrated to exert antitumor effects on multiple types of cancer. The current study aimed to investigate whether the potential inhibitory effects of CTD exist in human melanoma cells and to assess the underlying antitumor mechanisms of CTD. Using the Cell Counting Kit‑8 assay, it was demonstrated that CTD treatment reduced A375 cell proliferation significantly in a dose‑dependent manner. The colony formation assay demonstrated that CTD treatment could decrease the number of A375 cell colonies. Using subcutaneous xenograft tumor models, it was also demonstrated that CTD retarded solid tumor growth significantly. Furthermore, CTD treatment could induce A375 cell apoptosis, as detected by Annexin V‑fluorescein isothiocyanate/propidium iodide staining and western blot analysis. Notably, CTD treatment reduced microRNA (miR)‑21 expression and enhanced phosphatase and tensin homolog (PTEN) protein expression levels in A375 cells. Furthermore, overexpressing miR‑21 in A375 cells with the miR‑21 agomir blocked the antitumor effect of CTD both in vitro and in vivo. Finally, it was demonstrated that the inhibitory effects of CTD on A375 cells may be regulated by attenuating miR‑21‑mediated PTEN suppression. Based on these observations, it was suggested that CTD be used as a novel anti‑proliferation agent of human melanoma via targeting the miR‑21‑PTEN signaling pathway.