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 #202479
Title: Cinnamon polyphenols produce rapid G2/M arrest in a leukemic cell line

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

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 2/20/2007
Publication Date: 3/20/2007
Citation: Schoene, N.W., Kelly, M.A., Polansky, M.M., Anderson, R.A. 2007. Cinnamon polyphenols produce rapid G2/M arrest in a leukemic cell line. Journal of Federation of American Societies for Experimental Biology. 21:550.16.

Interpretive Summary: n/a

Technical Abstract: Water soluble polyphenols from cinnamon (CE) have been shown to have wide ranging effects on cellular signaling proteins that may ultimately result in decreased risk for insulin resistance, heart disease, and cancer. We recently demonstrated that treatment with CE for 24 h produced dose dependent arrests in the G2/M phase of the cell cycle in three leukemic cell lines. In a continuation of our experiments, we examined the short term effects on cell cycle progression in the CE-sensitive Jurkat cell line (Wurzburg, W). Cell cycle analyses were conducted on samples of treated (CE = 0.1mg/mL)versus non-treated W over 6 h. The percentages of cells in G2/M in CE-treated W increased significantly from 11.0 ± 1.0 to 23.6 ± 1.4 after 6 h, while the percentage for non-treated W remained essentially unchanged (12.3 ± 0.8). The increase in G2/M in CE-treated W correlated with an increase in volume measured electronically (from 866.0 ± 36.2 to 1021.0 ±34.2 fL). Samples of the cells were also fixed, permeabilized, and stained for detection of activated p38 MAPK by flow cytometry. After 4 h, there was a 26% increase in the activated phosphorylated form of this kinase in the CE-treated W compared to the non-treated control cells. Overall, these combined results provide additional evidence for the role of CE in regulating the kinase/phosphatase balance critical to a multitude of cellular signaling events.