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Journal of Cancer Prevention

Original Article

Cancer prevention research 2010; 15(2): 127-132

Published online June 30, 2010

© Korean Society of Cancer Prevention

Upregulation of p15INK4B Arrest G1/S Phase of Cell Cycle by Phosphorylation of SMAD3 in Մ-Tocotrienol Treated Human MDA-MB-231 Breast Cancer Cells

Jin-Soo Yoon and Gun-Do Kim

Abstract

Tocotrienols, a subgroup within the vitamin E family of compounds, have shown antiproliferative and anticancer properties. However, the molecular basis of these effects remains to be elucidated. In this study, the effect of Մ-Tocotrienol on cell cycle arrest was assessed by studying the levels of cyclin-dependent kinase 4 (CDK4), cyclin-dependant kinase 6 (CDK6), p15INK4B and other cell cycle controlling proteins in estrogen receptor-negative MDA-MB-231 breast cancer cells. The cell growth assay demonstrated that exposure of the MDA-MB-231 cells to Մ-Tocotrienol (25ՌM) resulted in a time-dependent inhibition of cell growth. The upregulation of p15INK4B can inhibit CDK4 and CDK6, which is responsible for the phosphorylation of retinoblastoma protein (Rb). In addition, p15INK4B can be controlled by phosphorylation of transcriptional factors called SMADs (Small Mothers Against Decapentaplegic). (Cancer Prev Res 15, 127-132, 2010)

Keywords: Tocotrienol, p15INK4B, MDA-MB-231, SMAD

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