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γ  -Tocotrienol is a natural vitamin E that displays potent anticancer activity, and previous studies suggest that these effects involve alterations in PPAR  γ   activity. Treatment with 0.5–6   μ  M    γ  -tocotrienol, 0.4–50   μ  M PPAR  γ   agonists (rosiglitazone or troglitazone), or 0.4–25   μ  M PPAR  γ   antagonists (GW9662 or T0070907) alone resulted in a dose-responsive inhibition of MCF-7 and MDA-MB-231 breast cancer proliferation. However, combined treatment of 1–4   μ  M    γ  -tocotrienol with PPAR  γ   agonists reversed the growth inhibitory effects of   γ  -tocotrienol, whereas combined treatment of 1–4   μ  M    γ  -tocotrienol with PPAR  γ   antagonists synergistically inhibited MCF-7 and MDA-MB-231 cell growth. Combined treatment of   γ  -tocotrienol and PPAR  γ   agonists caused an increase in transcription activity of PPAR  γ   along with increased expression of PPAR  γ   and RXR, and decrease in PPAR  γ   coactivators, CBP p/300, CBP C-20, and SRC-1, in both breast cancer cell lines. In contrast, combined treatment of   γ  -tocotrienol with PPAR  γ   antagonists resulted in a decrease in transcription activity of PPAR  γ  , along with decreased expression of PPAR  γ   and RXR, increase in PPAR  γ   coactivators, and corresponding decrease in PI3K/Akt mitogenic signaling in these cells. These findings suggest that elevations in PPAR  γ   are correlated with increased breast cancer growth and survival, and treatment that decreases PPAR  γ   expression may provide benefit in the treatment of breast cancer.

international journal of breast cancer

Mechanisms Mediating the Effects of<i>γ</i>-Tocotrienol When Used in Combination with PPAR<i>γ</i>Agonists or Antagonists on MCF-7 and MDA-MB-231 Breast Cancer Cells

Mechanisms Mediating the Effects ofγ-Tocotrienol When Used in Combination with PPARγAgonists or Antagonists on MCF-7 and MDA-MB-231 Breast Cancer Cells