J. Lipid Res.
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A more recent version of this article appeared on October 1, 2006

Papers In Press, published online ahead of print July 17, 2006
J. Lipid Res., doi:10.1194/jlr.M600269-JLR200
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Submitted on June 20, 2006
Revised on July 17, 2006
Accepted on July 17, 2006

Docosahexaenoic acid inhibits growth of mouse mammary cancer cells by interfering with p27/kip1, Cdk2, ERK1/ERK2 and retinoblastoma phosphorylation

Naim A. Khan, Kazuhiro Nishimura, Virginie Aires, Tomoko Yamashita, David Oaxaca-Castillo, Keiko Kashiwagi, and Kazuei Igarashi

Physiologie, Université de Bourgogne, Dijon 21000

Corresponding Author: Naim.Khan{at}u-bourgogne.fr

Docosahexaenoic acid (DHA), a polyunsaturated fatty acid of n-3 family, inhibited growth of FM3A mouse mammary cancer cells by arresting their progression from late-G1 to S phase of cell cycle. DHA upregulated p27Kip1 levels by inhibiting phosphorylation of mitogen-activated protein (MAP) kinases, i.e., ERK1/ERK2. Indeed, inhibition of ERK1/ERK2 phosphorylation by DHA, U0126 (chemical MEK inhibitor) and MEKSA (cells expressing dominant negative constructs of MEK) resulted in the accumulation of p27Kip1. MAPK inhibition by DHA did not increase p27Kip1 mRNA levels rather this fatty acid stabilized p27Kip1 contents and inhibited MAPK-dependent proteasomal degradation of this protein. DHA also diminished cyclin E phosphorylation, cyclin-dependent kinase 2 (CDK2) activity and phosphorylation of retinoblastoma protein (pRb) in these cells. Our study shows that DHA arrests cell growth by modulating the phosphorylation of cell cycle-related proteins.


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