A mechanistic study on the anti-cancer activity of ethyl caffeate in human ovarian cancer SKOV-3 cells

• Ethyl caffeate inhibits ovarian cancer cell proliferation, migration and invasion.
• Ethyl caffeate regulates mitogenic signaling pathways such as Akt, ERK and p38MAPK.
• Ethyl caffeate suppresses the expression of RTKs, integrin α3β1 and N-cadherin.

In the present study, we investigated the effect and molecular mechanism of ethyl caffeate (EC), a natural phenolic compound isolated from Ligularia fischeri, on human ovarian cancer cell proliferation and progression. EC-mediated inhibition of cell proliferation in SKOV-3 cells was accompanied by reduced expression of cell cycle-related proteins such as cyclin-dependent kinases and cyclins, resulting in pRb hypophosphorylation and G1 phase cell cycle arrest. Moreover, EC treatment markedly inhibited cell migration and invasion. These regulatory effects of EC on ovarian cancer cell proliferation, migration and invasion were associated with inactivation of mitogenic signaling pathways such as Akt, ERK and p38MAPK, and down-regulation of cell surface signaling molecules including receptor tyrosine kinases, integrin α3β1 and N-cadherin. Taken together, these findings suggest further evaluation and development of EC for the treatment and prevention of ovarian cancer.