Targeting PPARy signaling cascade for the prevention and treatment of prostate cancer
The peroxisome proliferator-activated receptor-gamma (PPARγ) is a member of the hormone-activated nuclear receptor superfamily. PPARγ can be activated by a diverse group of agents, such as endogenous polyunsaturated fatty acids, 15-deoxy- Δ 12,14-prostaglandin J2 (15d-PGJ2), and thiazolidinedione (T...
| Main Authors: | , , , |
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| Format: | Journal Article |
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Hindawi Publishing Corporation
2012
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| Online Access: | http://hdl.handle.net/20.500.11937/41438 |
| _version_ | 1848756146141134848 |
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| author | Sikka, S. Chen, L. Sethi, G. Kumar, Alan Prem |
| author_facet | Sikka, S. Chen, L. Sethi, G. Kumar, Alan Prem |
| author_sort | Sikka, S. |
| building | Curtin Institutional Repository |
| collection | Online Access |
| description | The peroxisome proliferator-activated receptor-gamma (PPARγ) is a member of the hormone-activated nuclear receptor superfamily. PPARγ can be activated by a diverse group of agents, such as endogenous polyunsaturated fatty acids, 15-deoxy- Δ 12,14-prostaglandin J2 (15d-PGJ2), and thiazolidinedione (TZD) drugs. PPARγ induces antiproliferative, antiangiogenic, and prodifferentiation pathways in several tissue types, thus making it a highly useful target for downregulation of carcinogenesis. These TZD-derived novel therapeutic agents, alone or in combination with other anticancer drugs, have translational relevance in fostering effective strategies for cancer treatment. TZDs have been proven for antitumor activity in a wide variety of experimental cancer models, both in vitro and in vivo, by affecting the cell cycle, inducing cell differentiation and apoptosis, as well as by inhibiting tumor angiogenesis. Angiogenesis inhibition mechanisms of TZDs include direct inhibition of endothelial cell proliferation and migration, as well as reduction in tumor cell vascular endothelial growth factor production. In prostate cancer, PPARγ ligands such as troglitazone and 15d-PGJ2 have also shown to inhibit tumor growth. This paper will focus on current discoveries in PPARγ activation, targeting prostate carcinogenesis as well as the role of PPARγ as a possible anticancer therapeutic option. Here, we review PPARγ as an antitumor agent and summarize the antineoplastic effects of PPARγ agonists in prostate cancer. |
| first_indexed | 2025-11-14T09:07:33Z |
| format | Journal Article |
| id | curtin-20.500.11937-41438 |
| institution | Curtin University Malaysia |
| institution_category | Local University |
| last_indexed | 2025-11-14T09:07:33Z |
| publishDate | 2012 |
| publisher | Hindawi Publishing Corporation |
| recordtype | eprints |
| repository_type | Digital Repository |
| spelling | curtin-20.500.11937-414382017-09-13T16:05:31Z Targeting PPARy signaling cascade for the prevention and treatment of prostate cancer Sikka, S. Chen, L. Sethi, G. Kumar, Alan Prem The peroxisome proliferator-activated receptor-gamma (PPARγ) is a member of the hormone-activated nuclear receptor superfamily. PPARγ can be activated by a diverse group of agents, such as endogenous polyunsaturated fatty acids, 15-deoxy- Δ 12,14-prostaglandin J2 (15d-PGJ2), and thiazolidinedione (TZD) drugs. PPARγ induces antiproliferative, antiangiogenic, and prodifferentiation pathways in several tissue types, thus making it a highly useful target for downregulation of carcinogenesis. These TZD-derived novel therapeutic agents, alone or in combination with other anticancer drugs, have translational relevance in fostering effective strategies for cancer treatment. TZDs have been proven for antitumor activity in a wide variety of experimental cancer models, both in vitro and in vivo, by affecting the cell cycle, inducing cell differentiation and apoptosis, as well as by inhibiting tumor angiogenesis. Angiogenesis inhibition mechanisms of TZDs include direct inhibition of endothelial cell proliferation and migration, as well as reduction in tumor cell vascular endothelial growth factor production. In prostate cancer, PPARγ ligands such as troglitazone and 15d-PGJ2 have also shown to inhibit tumor growth. This paper will focus on current discoveries in PPARγ activation, targeting prostate carcinogenesis as well as the role of PPARγ as a possible anticancer therapeutic option. Here, we review PPARγ as an antitumor agent and summarize the antineoplastic effects of PPARγ agonists in prostate cancer. 2012 Journal Article http://hdl.handle.net/20.500.11937/41438 10.1155/2012/968040 Hindawi Publishing Corporation fulltext |
| spellingShingle | Sikka, S. Chen, L. Sethi, G. Kumar, Alan Prem Targeting PPARy signaling cascade for the prevention and treatment of prostate cancer |
| title | Targeting PPARy signaling cascade for the prevention and treatment of prostate cancer |
| title_full | Targeting PPARy signaling cascade for the prevention and treatment of prostate cancer |
| title_fullStr | Targeting PPARy signaling cascade for the prevention and treatment of prostate cancer |
| title_full_unstemmed | Targeting PPARy signaling cascade for the prevention and treatment of prostate cancer |
| title_short | Targeting PPARy signaling cascade for the prevention and treatment of prostate cancer |
| title_sort | targeting ppary signaling cascade for the prevention and treatment of prostate cancer |
| url | http://hdl.handle.net/20.500.11937/41438 |