ethyl-caffeate and Ovarian-Neoplasms

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 p38(MAPK), 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.

Topics: Blotting, Western; Caffeic Acids; Cell Cycle; Cell Line, Tumor; Cell Proliferation; Cyclin-Dependent Kinases; Cyclins; Extracellular Signal-Regulated MAP Kinases; Female; Gene Expression Regulation, Neoplastic; Humans; Ovarian Neoplasms; p38 Mitogen-Activated Protein Kinases; Proto-Oncogene Proteins c-akt; Retinoblastoma Protein; Reverse Transcriptase Polymerase Chain Reaction; RNA, Neoplasm; Signal Transduction