Esterification of p-Coumaric Acid Improves the Control over Melanoma Cell Growth

Previous studies reported that p-coumaric acid modulates melanoma growth. Because the esterification of p-coumaric acid (p-CA) enhanced its activity as an antimelanogenic agent, we aimed to determine the antitumor potential of two derivatives, the ethyl and butyl esters, against the murine B16-F10 and the human SK-MEL-25 melanoma cells. Cell viability was determined in vitro by the lactate dehydrogenase release and violet crystal absorption assays. The cell proliferation rate and cell cycle behavior were determined by the colony formation assay and flow cytometry analysis. Although p-CA, at the concentration of 1 mM, failed to exert a significant antitumor activity, the ethyl and butyl ester derivatives caused substantial tumor cell death at doses < 1 mM. Despite a reduction in their direct cytotoxicity at minor doses, both products controlled the melanoma growth by arresting the cell cycle at the G0/G1 (B16-F10) or S/G2 (SK-MEL-25). Furthermore, the in vivo experiments showed that the butyl ester derivative suppressed the lung B16-F10 burden, compared to the p-CA-treated mice. Thus, the esterification of p-coumaric acid improved the control over the proliferation of murine and human melanoma cells and can be considered an approach for designing novel anticancer agents.

Automated summary

The esterification of p-coumaric acid enhanced its activity as an antimelanogenic agent against melanoma cells. The ethyl and butyl ester derivatives of p-coumaric acid showed significant antitumor potential at doses below 1 mM. They controlled melanoma growth by arresting the cell cycle of the B16-F10 and SK-MEL-25 cells. The butyl ester derivative also suppressed lung B16-F10 burden in vivo compared to p-coumaric acid treatment.