the ppar gamma agonist troglitazone regulates erk 12 phosphorylation via a pparγ-independent, mek-dependent pathway in human prostate cancer cellspparγ受体激动剂troglitazone调节erk 12磷酸化通过pparγ-independent mek-dependent通路在人类前列腺癌细胞.pdfVIP

Hindawi Publishing Corporation PPAR Research Volume 2012, Article ID 929052, 9 pages doi:10.1155/2012/929052 Research Article The PPAR Gamma Agonist Troglitazone Regulates Erk 1/2 Phosphorylation via a PPARγ-Independent, MEK-Dependent Pathway in Human Prostate Cancer Cells Adrienne Bolden,1 Lynikka Bernard,1 Danielle Jones,1 Tunde Akinyeke,1, 2 and LaMonica V. Stewart1 1 Department of Biochemistry and Cancer Biology, Meharry Medical College, Nashville, TN 37208, USA 2 Basic Science and Craniofacial Biology, New York University College of Dentistry, 345 East 24th Street, New York City, NY 10010, USA Correspondence should be addressed to LaMonica V. Stewart, lstewart@ Received 1 September 2011; Revised 22 November 2011; Accepted 23 November 2011 Academic Editor: R. P. Phipps Copyright © 2012 Adrienne Bolden et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Thiazolidinediones (TZDs) dramatically reduce the growth of human prostate cancer cells in vitro and in vivo. To determine whether the antitumor effects of TZDs were due in part to changes in the MEK/Erk signaling pathway, we examined the regulation of Erk phosphorylation by the TZD troglitazone within the PC-3 and C4-2 human prostate cancer cell lines. Western blot analysis revealed troglitazone-induced phosphorylation of Erk in both PC-3 and C4-2 cells. Troglitazone-induced increases in Erk phos- phorylation were suppressed by the MEK inhibitor U0126 but not by the PPARγ antagonist GW9662. Pretreatment with U0126 did not alter the ability of troglitazone to regulate expression of two proteins that control cell cycle, p21, an