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Peroxisome Proliferator-Activated Receptor γ (PPARγ)-Independent Antitumor Effect of Thiazolidinediones

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2009, Doctor of Philosophy, Ohio State University, Pharmacy.
We verified that the antitumor effects of thiazolidinediones involve PPARγ-independent mechanisms and demonstrated for the first time that these agents also function as energy restriction mimetics. Thiazolidinediones elicit several hallmark energy restriction-associated responses, including elevation of Sirt1, ER stress, beta-TrCP, and autophagy, and activation of AMPK. Activation of the Sirt1-CSN5-Skp2-beta-TrCP cascade was shown to mediate thiazolidinedione- or ERMA-induced apoptosis, while the AMPK-TSC1/2-mTOR-p70S6K pathway was shown to account for the induction of autophagy. However, the role of ER stress induction in thiazolidinedione- or ERMA-treated cancer cells remains unclear
Ching-Shih Chen (Advisor)
Li Pui-Kai (Tom) (Committee Member)
Oberyszyn Tatiana (Committee Member)
Ringel Matthew (Committee Member)
152 p.

Recommended Citations

Citations

  • Wei, S. (2009). Peroxisome Proliferator-Activated Receptor γ (PPARγ)-Independent Antitumor Effect of Thiazolidinediones [Doctoral dissertation, Ohio State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=osu1259167390

    APA Style (7th edition)

  • Wei, Shuo. Peroxisome Proliferator-Activated Receptor γ (PPARγ)-Independent Antitumor Effect of Thiazolidinediones. 2009. Ohio State University, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=osu1259167390.

    MLA Style (8th edition)

  • Wei, Shuo. "Peroxisome Proliferator-Activated Receptor γ (PPARγ)-Independent Antitumor Effect of Thiazolidinediones." Doctoral dissertation, Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1259167390

    Chicago Manual of Style (17th edition)