Category Archives: B16 (lung metastasis)

Acetoside

Cancer: Lung cancer, melanoma

Action: Anti-metastatic

Acetoside is isolated from Stachys sieboldii (Miq), Arctostaphylos uva-ursi [(L.) Spreng, Cistanche deserticola (Ma).

Anti-metastatic; Lung Cancer

The anti-metastatic effect of acteoside, a phenylethanoid glycoside widely distributed in the plant kingdom, was examined with respect to lung metastasis using a mouse model injected with B16 melanoma cells intravenously. Administration of acteoside prolonged survival time significantly and the average survival time was 63.3 +/- 3.4d compared with 52.1 +/- 2.5d in control mice. This result suggests that acteoside showed suppressive effect on lung metastasis of B16 melanoma cells (Ohno et al., 2009).

Melanoma

Acteoside showed an inhibitory effect on tyrosinase activity and melanin synthesis in both cell-free assay systems and cultured B16F10 melanoma cells. Acteoside decreased levels of tyrosinase, tyrosinase-related protein-1 (TRP-1) and microphthalmia-associated transcription factor (MITF) proteins, whereas it increased ERK phosphorylation. Acteoside suppressed melanogenesis induced by α-melanocyte-stimulating hormone and showed UV-absorbing effects (Son et al., 2011). Acteoside also inhibited production of both melanin and cyclic AMP in cells stimulated by 1 micromol/l forskolin, an adenyl cyclase activator. Acteoside showed anti-oxidant activity in a cell-free DPPH (1-diphenyl-2-picrylhydroazyl) assay and inhibited generation of intracellular reactive oxygen species (Song & Sim., 2009).

References

Ohno T, Inoue M, Ogihara Y, Saracoglu I. (2012). Anti-metastatic activity of acteoside, a phenylethanoid glycoside. Biological & Pharmaceutical Bulletin, 25(5):666-8. doi: 10.1248/bpb.25.666


Song HS, Sim SS. (2009). Acteoside inhibits alpha-MSH-induced melanin production in B16 melanoma cells by inactivation of adenyl cyclase. J Pharm Pharmacol, 61(10):1347-51. doi: 10.1211/jpp/61.10.0011.


Son YO, Lee SA, Kim SS, et al. (2011). Acteoside inhibits melanogenesis in B16F10 cells through ERK activation and tyrosinase down-regulation. J Pharm Pharmacol, 63(10):1309-19. doi: 10.1111/j.2042-7158.2011.01335.x.