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Volume 2011 (2011), Article ID 171765, 11 pages
Promotes Growth and Invasion of Thyroid Cancer Cells
1Division of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Colorado Denver, Aurora, CO 80045, USA
2University of Colorado Cancer Center, University of Colorado Denver, Aurora, CO 80045, USA
Received 9 August 2011; Accepted 17 September 2011
Academic Editor: Maria Paola Cerù
Copyright © 2011 William M. Wood 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.
- T. M. Willson, P. J. Brown, D. D. Sternbach, and B. R. Henke, “The PPARs: from orphan receptors to drug discovery,” Journal of Medicinal Chemistry, vol. 43, no. 4, pp. 527–550, 2000.
- W. Wahli, O. Braissant, and B. Desvergne, “Peroxisome proliferator activated receptors: transcriptional regulators of adipogenesis, lipid metabolism and more,” Chemistry and Biology, vol. 2, no. 5, pp. 261–266, 1995.
- P. A. Grimaldi, “The roles of PPARs in adipocyte differentiation,” Progress in Lipid Research, vol. 40, no. 4, pp. 269–281, 2001.
- P. Tontonoz, S. Singer, B. M. Forman et al., “Terminal differentiation of human liposarcoma cells induced by ligands for peroxisome proliferator-activated receptor γ and the retinoid X receptor,” Proceedings of the National Academy of Sciences of the United States of America, vol. 94, no. 1, pp. 237–241, 1997.
- P. Sarraf, E. Mueller, D. Jones et al., “Differentiation and reversal of malignant changes in colon cancer through PPARγ,” Nature Medicine, vol. 4, no. 9, pp. 1046–1052, 1998.
- Y. Bren-Mattison, V. Van Putten, D. Chan, R. Winn, M. W. Geraci, and R. A. Nemenoff, “Peroxisome proliferator-activated receptor-γ (PPARγ) inhibits tumorigenesis by reversing the undifferentiated phenotype of metastatic non-small-cell lung cancer cells (NSCLC),” Oncogene, vol. 24, no. 8, pp. 1412–1422, 2005.
- V. G. Keshamouni, R. C. Reddy, D. A. Arenberg et al., “Peroxisome proliferator-activated receptor-γ activation inhibits tumor progression in non-small-cell lung cancer,” Oncogene, vol. 23, no. 1, pp. 100–108, 2004.
- B. Seed, “PPARγ and colorectal carcinoma: conflicts in a nuclear family,” Nature Medicine, vol. 4, no. 9, pp. 1004–1005, 1998.
- A. Abe, Y. Kiriyama, M. Hirano et al., “Troglitazone suppresses cell growth of KU812 cells independently of PPARγ,” European Journal of Pharmacology, vol. 436, no. 1-2, pp. 7–13, 2002.
- S. Wei, J. Yang, S. L. Lee, S. K. Kulp, and C. S. Chen, “PPARγ-independent antitumor effects of thiazolidinediones,” Cancer Letters, vol. 276, no. 2, pp. 119–124, 2009.
- K. Ohta, T. Endo, K. Haraguchi, J. M. Hershman, and T. Onaya, “Ligands for peroxisome proliferator-activated receptor γ inhibit growth and induce apoptosis of human papillary thyroid carcinoma cells,” Journal of Clinical Endocrinology and Metabolism, vol. 86, no. 5, pp. 2170–2177, 2001.
- M. L. Martelli, R. Iuliano, I. Le Pera et al., “Inhibitory effects of peroxisome proliferator-activated receptor γ on thyroid carcinoma cell growth,” Journal of Clinical Endocrinology and Metabolism, vol. 87, no. 10, pp. 4728–4735, 2002.
- J. W. Park, R. Zarnegar, H. Kanauchi et al., “Troglitazone, the peroxisome proliferator-activated receptor-γ agonist, induces antiproliferation and redifferentiation in human thyroid cancer cell lines,” Thyroid, vol. 15, no. 3, pp. 222–231, 2005.
- A. Aiello, G. Pandini, F. Frasca et al., “Peroxisomal proliferator-activated receptor-γ agonists induce partial reversion of epithelial-mesenchymal transition in anaplastic thyroid cancer cells,” Endocrinology, vol. 147, no. 9, pp. 4463–4475, 2006.
- J. A. Copland, L. A. Marlow, S. Kurakata et al., “Novel high-affinity PPARγ agonist alone and in combination with paclitaxel inhibits human anaplastic thyroid carcinoma tumor growth via ,” Oncogene, vol. 25, no. 16, pp. 2304–2317, 2006.
- R. E. Schweppe, J. P. Klopper, C. Korch et al., “Deoxyribonucleic acid profiling analysis of 40 human thyroid cancer cell lines reveals cross-contamination resulting in cell line redundancy and misidentification,” Journal of Clinical Endocrinology and Metabolism, vol. 93, no. 11, pp. 4331–4341, 2008.
- J. P. Klopper, V. Sharma, A. Berenz et al., “Retinoid and thiazolidinedione therapies in melanoma: an analysis of differential response based on nuclear hormone receptor expression,” Molecular Cancer, vol. 8, article 16, 2009.
- J. P. Klopper, A. Berenz, W. R. Hays et al., “In vivo and microarray analysis of rexinoid-responsive anaplastic thyroid carcinoma,” Clinical Cancer Research, vol. 14, no. 2, pp. 589–596, 2008.
- E. Kebebew, M. Peng, E. Reiff et al., “A phase II trial of rosiglitazone in patients with thyroglobulin-positive and radioiodine-negative differentiated thyroid cancer,” Surgery, vol. 140, no. 6, pp. 960–966, 2006.
- J. C. Philips, C. Petite, J. P. Willi, F. Buchegger, and C. A. Meier, “Effect of peroxisome proliferator-activated receptor γ agonist, rosiglitazone, on dedifferentiated thyroid cancers,” Nuclear Medicine Communications, vol. 25, no. 12, pp. 1183–1186, 2004.
- L. A. Marlow, L. A. Reynolds, A. S. Cleland et al., “Reactivation of suppressed RhoB is a critical step for the inhibition of anaplastic thyroid cancer growth,” Cancer Research, vol. 69, no. 4, pp. 1536–1544, 2009.
- K. B. Ain, “Management of undifferentiated thyroid cancer,” Baillieres Best Practice and Research: Clinical Endocrinology and Metabolism, vol. 14, no. 4, pp. 615–629, 2000.
- M. N. Nikiforova, P. W. Biddinger, C. M. Caudill, T. G. Kroll, and Y. E. Nikiforov, “PAX8-PPARγ rearrangement in thyroid tumors: RT-PCR and immunohistochemical analyses,” The American Journal of Surgical Pathology, vol. 26, no. 8, pp. 1016–1023, 2002.
- M. A. Aldred, C. Morrison, O. Gimm et al., “Peroxisome proliferator-activated receptor gamma is frequently downregulated in a diversity of sporadic nonmedullary thyroid carcinomas,” Oncogene, vol. 22, no. 22, pp. 3412–3416, 2003.
- S. Karger, K. Berger, M. Eszlinger et al., “Evaluation of peroxisome proliferator-activated receptor-γ expression in benign and malignant thyroid pathologies,” Thyroid, vol. 15, no. 9, pp. 997–1003, 2005.
- N. Hayashi, S. Nakamori, N. Hiraoka et al., “Antitumor effects of peroxisome proliferator activate receptor gamma ligands on anaplastic thyroid carcinoma,” International Journal of Oncology, vol. 24, no. 1, pp. 89–95, 2004.
- J. Yu, B. Shen, E. S. H. Chu et al., “Inhibitory role of peroxisome proliferator-activated receptor gamma in hepatocarcinogenesis in mice and in vitro,” Hepatology, vol. 51, no. 6, pp. 2008–2019, 2010.
- C. A. McAlpine, Y. Barak, I. Matise, and R. T. Cormier, “Intestinal-specific PPARγ deficiency enhances tumorigenesis in mice,” International Journal of Cancer, vol. 119, no. 10, pp. 2339–2346, 2006.
- Y. Kato, H. Ying, L. Zhao et al., “PPARγ insufficiency promotes follicular thyroid carcinogenesis via activation of the nuclear factor-κB signaling pathway,” Oncogene, vol. 25, no. 19, pp. 2736–2747, 2006.
- E. Saez, J. Rosenfeld, A. Livolsi et al., “PPARγ signaling exacerbates mammary gland tumor development,” Genes and Development, vol. 18, no. 5, pp. 528–540, 2004.
- H. V. Reddi, P. Madde, D. Milosevic et al., “The putative PAX8/PPARγ fusion oncoprotein exhibits partial tumor suppressor activity through Up-regulation of Micro-RNA-122 and dominant-negative PPARγ activity,” Genes & Cancer, vol. 2, no. 1, pp. 46–55, 2011.
- C. H. Yam, T. K. Fung, and R. Y. C. Poon, “Cyclin A in cell cycle control and cancer,” Cellular and Molecular Life Sciences, vol. 59, no. 8, pp. 1317–1326, 2002.
- H. Kawamoto, H. Koizumi, and T. Uchikoshi, “Expression of the G2-M checkpoint regulators cyclin B1 and cdc2 in nonmalignant and malignant human breast lesions: immunocytochemical and quantitative image analyses,” The American Journal of Pathology, vol. 150, no. 1, pp. 15–23, 1997.
- S. H. Chung, N. Onoda, T. Ishikawa et al., “Peroxisome proliferator-activated receptor gamma activation induces cell cycle arrest via the p53-independent pathway in human anaplastic thyroid cancer cells,” Japanese Journal of Cancer Research, vol. 93, no. 12, pp. 1358–1365, 2002.
- D. Bonofiglio, H. Qi, S. Gabriele et al., “Peroxisome proliterator-activated receptor γ inhibits follicular and anaplastic thyroid carcinoma cells growth by upregulating gene in a Sp1-dependent manner,” Endocrine-Related Cancer, vol. 15, no. 2, pp. 545–557, 2008.
- L. Fajas, V. Egler, R. Reiter, S. Miard, A. M. Lefebvre, and J. Auwerx, “PPARγ controls cell proliferation and apoptosis in an RB-dependent manner,” Oncogene, vol. 22, no. 27, pp. 4186–4193, 2003.
- R. F. Morrison and S. R. Farmer, “Role of PPARγ in regulating a cascade expression of cyclin-dependent kinase inhibitors, and , during adipogenesis,” Journal of Biological Chemistry, vol. 274, no. 24, pp. 17088–17097, 1999.
- A. Itami, G. Watanabe, Y. Shimada et al., “Ligands for peroxisome proliferator-activated receptor γ inhibit growth of pancreatic cancers both in vitro and in vivo,” International Journal of Cancer, vol. 94, no. 3, pp. 370–376, 2001.
- H. Liu, C. Zang, M. H. Fenner, K. Possinger, and E. Elstner, “PPARγ ligands and ATRA inhibit the invasion of human breast cancer cells in vitro,” Breast Cancer Research and Treatment, vol. 79, no. 1, pp. 63–74, 2003.
- Y. C. Yang, T. C. Ho, S. L. Chen, H. Y. Lai, J. W. Wu, and Y. P. Tsao, “Inhibition of cell motility by troglitazone in human ovarian carcinoma cell line,” BMC Cancer, vol. 7, article 216, 2007.
- R. Coras, A. Hölsken, S. Seufert et al., “The peroxisome proliferator-activated receptor-γ agonist troglitazone inhibits transforming growth factor-β-mediated glioma cell migration and brain invasion,” Molecular Cancer Therapeutics, vol. 6, no. 6, pp. 1745–1754, 2007.