Submitted to: Cancer Letters
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 23, 2004
Publication Date: May 5, 2005
Citation: Schoene, N.W., Kelly, M.A., Polansky, M.M., Anderson, R.A. 2005. Water soluble polymeric polyphenols from cinnamon inhibit proliferation and alter cell cycle distribution patterns of hematologic tumor cell lines. Cancer Letters. 230:134-140. Interpretive Summary: Both epidemiological and laboratory studies have produced data in support of the health promoting effects of polyphenolic compounds found in plants. However, little is known about the processes whereby these constituents reduce the risk of chronic diseases such as cancer and heart disease. We have isolated and characterized water soluble components from cinnamon that causes cells to have a more sensitive response to insulin changing the signaling circuitry. To expand understanding of how these compounds affect cellular responses related to chronic diseases, we studied the effect of this extract on tumor cells grown in culture. The extract reduced proliferation with increased doses and caused significant shifts in the patterns of DNA synthesis in the cells. These results suggest that the extract can interact with the proteins that regulate growth-promoting signals to produce tumor suppression. This additional information about possible mechanisms of action to explain the benefits of dietary plant polyphenols will benefit nutrition and cancer researchers and dietitians.
Technical Abstract: To explore possible anti-cancer properties of water-soluble, polymeric polyphenols from cinnamon, three myeloid cell lines (Jurkat, Wurzburg, U937) were exposed to increasing concentrations of an aqueous extract prepared from cinnamon (CE) for 24 h. Cell growth and cell cycle distribution patterns responded in a dose-dependent manner to CE. A significant increase of the percentage of cells distributed in G2/M was observed in all three cell lines as the amount of CE increased. At the highest dose of CE, the percentage of Wurzburg cells,in G2/M was 1.5 and 2.0 fold higher than those observed for Jurkat and U937 cells, respectively. Wurzburg cells lack the CD45 phosphatase and may be more sensitive to imbalances in signaling through kinase/phosphatase networks that promote growth. The results suggest the potential of CE to interact with phosphorylation/dephosphorylation signaling activities ro reduce cellular proliferation in tandem with a block at the G2/M phase of the cell cycle.