S-petasin induces apoptosis and inhibits cell migration through activation of p53 pathway signaling in melanoma B16F10 cells and A375 cells

Melanoma is a dangerous type of skin cancer that develops from the melanocytes. Activation of p53 in melanoma cells has been validated as a strategy for melanoma therapy. S-Petasin, a dietary sesquiterpene isolated from Petasites japonicus, has been shown to possess multiple biological effects. However, no studies have reported that s-petasin exerted anti-melanoma or inhibited activity in melanoma cells. We investigated the effect of s-petasin in B16F10 cells and A375 cells and the underlying molecular mechanism. S-Petasin exerted a significant anti-proliferation effect on B16F10 cells and A375 cells as measured by the MTT assay and crystal violet staining assay. S-Petasin induced B16F10 and A375 cells apoptosis as evidenced by flow cytometry assay and western blot assay. Wound healing assay and transwell cell migration and invasion assay revealed that s-petasin suppressed B16F10 and A375 cells migration in vitro. For mechanism study, western blot assay indicated that s-petasin activated the p53 pathway signaling. Furthermore, expression of Bcl-2, Bcl-_XL, Bax, MMP-2, MMP-9, p21, CDK4 and cyclin D₁ were regulated by s-petasin. Taken together, our data suggest that s-petasin is a novel compound which can induce apoptosis and inhibit cell migration through activation of the p53 pathway signaling in melanoma B16F10 and A375 cells.

Keywords: A375 cells; B16F10 cells; Cell apoptosis; Cell migration; p53; s-Petasin.