Skip to main content
ARS Home » Northeast Area » Beltsville, Maryland (BHNRC) » Beltsville Human Nutrition Research Center » Diet, Genomics and Immunology Laboratory » Research » Publications at this Location » Publication #155975
Title: POLYMERIC POLYPHENOLS IN CINNAMON INHIBIT TUMOR CELL PROLIFERATION WITH ARREST AT G2/M

Author
item Kelly, Meghan
item Schoene, Norberta
item Polansky, Marilyn
item Anderson, Richard

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 11/12/2003
Publication Date: 4/11/2004
Citation: Kelly, M.A., Schoene, N.W., Polansky, M.M., Anderson, R.A. 2004. Polymeric polyphenols in cinnamon inhibit tumor cell proliferation with arrest at g2/m [abstract]. Federation of American Society of Experimental Biology. 18:A591.3-A886.

Interpretive Summary:

Technical Abstract: We recently demonstrated that water soluble, polymeric polyphenols extracted from cinnamon (CE) possess insulin potentiating activity by regulating kinase/phosphatase signaling activities. These enzymes also act at key control points throughout the cell cycle and are potential targets for regulation of tumor cell growth. To explore possible chemo-preventive properties of these polyphenols, three cell lines [Jurkat (J), CD45- Jurkat (W), U937 (U)] were treated with 0.0, 0.05, 0.075, 0.10, and 0.20 mg/mL CE. After 24h, cells were counted, fixed in ethanol, stained for DNA content, and analyzed by flow cytometry. Cell growth and changes in cell cycle distribution patterns for the three cell lines responded to CE in a dose responsive manner. W, with a different signaling balance because of the lack of CD45 phosphatase, demonstrated significantly increased sensitivity to CE at steps regulating G2/M compared to J and U. The following percentage distribution of cells in G2/M was observed after 24 h with 0.20 mg/mL CE (SEM, n=4): J, 51%; W, 83%; U, 41% (0.0 CE = ~12% for the cell lines). Phosphorylation of MAPK p38 correlated positively with percentage of cells in G2/M. In summary, the results show that CE inhibited tumor cell growth with arrest at G2/M by modulating kinase/phosphatase signaling activities. Thus, depending on the cellular context, CE can act as either chemo-preventive agent or insulin mimetic.