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Previous findings showed that the anticancer effects of combined   γ  -tocotrienol and peroxisome proliferator activated receptor   γ   (PPAR  γ  ) antagonist treatment caused a large reduction in PPAR  γ   expression. However, other studies suggest that the antiproliferative effects of   γ  -tocotrienol and/or PPAR  γ   antagonists are mediated, at least in part, through PPAR  γ  -independent mechanism(s). Studies were conducted to characterize the role of PPAR  γ   in mediating the effects of combined treatment of   γ  -tocotrienol with PPAR  γ   agonists or antagonists on the growth of PPAR  γ   negative +SA mammary cells and PPAR  γ  -positive and PPAR  γ  -silenced MCF-7 and MDA-MB-231 breast cancer cells. Combined treatment of   γ  -tocotrienol with PPAR  γ   antagonist decreased, while combined treatment of   γ  -tocotrienol with PPAR  γ   agonist increased, growth of all cancer cells. However, treatment with high doses of 15d-PGJ 2 , an endogenous natural ligand for PPAR  γ  , had no effect on cancer cell growth. Western blot and qRT-PCR studies showed that the growth inhibitory effects of combined   γ  -tocotrienol and PPAR  γ   antagonist treatment decreased cyclooxygenase (COX-2), prostaglandin synthase (PGDS), and prostaglandin D 2  (PGD 2 ) synthesis. In conclusion, the anticancer effects of combined   γ  -tocotrienol and PPAR  γ   antagonists treatment in PPAR  γ   negative/silenced breast cancer cells are mediated through PPAR  γ  -independent mechanisms that are associated with a downregulation in COX-2, PGDS, and PGD 2  synthesis.

ppar research

Synergistic Antiproliferative Effects of Combinedγ-Tocotrienol and PPARγAntagonist Treatment Are Mediated through PPARγ-Independent Mechanisms in Breast Cancer Cells