Abstract #961: Anti-proliferative activity of apigenin in colorectal and breast cancer cells

Flavonoids, a group of naturally occurring compounds widely distributed in nature, are ubiquitous in vegetables, berries, and fruits, and fortunately even in chocolate. Among tested flavonoids (Phloridzin, Quercetin, Kaempferol, Naringenin, Luteolin, Pelargonidin, Daidzin, Daidzein, Glycitin, Glycitein, Genistin, Genistein and Apigenin), apigenin showed to be the most promising compound in halting cancer cell growth. Many laboratories, including ours, have reported persuasive evidence of beneficial effects of plant-derived compounds in cancers of the gastrointestinal tract, lung, skin, prostate, and breast. Since conventional therapeutic and surgical approaches have not been able to fully control the incidence and outcome of most cancer types, including colorectal and breast neoplasia, there is an urgent need to develop mechanism-based approaches for the management of cancer. Apigenin is a non-mutagenic flavonoid found in vegetables and fruits, including parsley, onions, wheat sprouts, chamomile, seasonings, tea and oranges, and has cancer preventive activity. Apigenin has been reported to act via several mechanisms, including promotion of cell cycle arrest and apoptosis, inhibition of mutagenesis, and suppression of signal transduction. It has been also reported that apigenin induces ERK and p38MAPK, but had little effect on the Jun kinase activity in HCT-116 cells. However, the molecular targets of apigenin have not been elucidated in details. In this study, we were examined several protein involved in apoptosis and tumorigenesis. We found that the expression of pro-apoptotic protein NAG-1 and cell cycle regulator cyclin D1 were altered in human colorectal and breast cancer cells. Apigenin also affects other proteins involved in \#946;-catenin signaling pathway and kinase pathways in human colorectal and breast cancer cells. This information may lead to the rational design of more effective anti-cancer agents and help justify clinical trials as well as further clarify apigenin\#8217;s mechanisms of action. (This is supported by NIH, ACS, and the Royal Golden Jubilee Ph.D. Program, PHD/0245/2545)

Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 961.