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

• Published in: Chemico-biological interactions 2014-08, Vol.219, p.151-158
• Main Authors: Lee, Ha Neul, Kim, Jin-Kyu, Kim, Jae Hyeon, Lee, Sang-Jin, Ahn, Eun-Kyung, Oh, Joa Sub, Seo, Dong-Wan
• Format: Article
• Language: English
• Subjects: Blotting, Western; Caffeic Acids - pharmacology; Caffeic Acids - therapeutic use; Cell Cycle - physiology; Cell Line, Tumor; Cell Proliferation - drug effects; Cyclin-Dependent Kinases - metabolism; Cyclins - metabolism; Ethyl caffeate; Extracellular Signal-Regulated MAP Kinases - metabolism; Female; Gene Expression Regulation, Neoplastic - physiology; Humans; Integrin α3β1; Ligularia fischeri; Ovarian cancer; Ovarian Neoplasms - drug therapy; Ovarian Neoplasms - enzymology; Ovarian Neoplasms - genetics; p38 Mitogen-Activated Protein Kinases - metabolism; Proto-Oncogene Proteins c-akt - metabolism; Receptor tyrosine kinase; Retinoblastoma Protein - metabolism; Reverse Transcriptase Polymerase Chain Reaction; RNA, Neoplasm - chemistry; RNA, Neoplasm - genetics; Signal Transduction - physiology
• ISSN: 0009-2797; 1872-7786
• DOI: 10.1016/j.cbi.2014.05.017

•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.