beta-escin and Melanoma

β-Escin, a natural triterpene saponin was extracted from Aesculus hippocastanum seeds, which have been widely used to treat inflammation in traditional medicine. In an effort to study the possible anti-tumor effects of β-escin, we performed wound healing, invasion, and adhesion assays to examine the effects of β-escin on cell migration, invasion, and angiogenesis. Our results revealed that β-escin inhibits cell migration as well as motility in B16F10 and SK-MEL5 cells in a dose-dependent manner. RT-PCR and Western blot analysis showed that β-escin increased TIMP-1, -2 while significantly downregulated phosphorylated extracellular signal-regulated kinase (p-ERK) expression, and suppressing nuclear factor-kappa B (NF-κB) and inhibitor of nuclear factor-kappa B (IκB) expression. Overall, the data from the current study suggest that β-escin has the potential for inhibiting both metastatic and angiogenic activities, and are the earliest evidence for the involvement of the NF-κB/IκB signaling in β-escin-induced anti-tumor effects.

Topics: Aesculus; Animals; Antineoplastic Agents, Phytogenic; Apoptosis; Cell Line, Tumor; Cell Movement; Cell Proliferation; Down-Regulation; Escin; Extracellular Signal-Regulated MAP Kinases; Humans; I-kappa B Proteins; MAP Kinase Signaling System; Melanoma; Mice; NF-kappa B; Phosphorylation; Phytotherapy; Plant Extracts; Seeds; Signal Transduction