Peroxisome proliferator-activated receptor δ and γ agonists differentially alter tumor differentiation and progression during mammary carcinogenesis
Peroxisome proliferator-activated receptor (PPAR) represents a ligand-dependent nuclear receptor family that regulates multiple metabolic processes associated with fatty acid beta-oxidation, glucose utilization, and cholesterol transport. These and other receptor-mediated actions pertain to their ro...
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| Published in | Cancer research (Chicago, Ill.) Vol. 65; no. 9; pp. 3950 - 3957 |
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| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Philadelphia, PA
American Association for Cancer Research
01.05.2005
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Peroxisome proliferator-activated receptor (PPAR) represents a ligand-dependent nuclear receptor family that regulates multiple metabolic processes associated with fatty acid beta-oxidation, glucose utilization, and cholesterol transport. These and other receptor-mediated actions pertain to their role in hypolipidemic and antidiabetic therapies and as potential targets for cancer chemopreventive agents. The present study evaluated the chemopreventive activity of two highly potent and selective PPARgamma and PPARdelta agonists in a progestin- and carcinogen-induced mouse mammary tumorigenesis model. Animals treated with the PPARgamma agonist GW7845 exhibited a moderate delay in tumor formation. In contrast, animals treated with the PPARdelta agonist GW501516 showed accelerated tumor formation. Significantly, tumors from GW7845-treated mice were predominantly ductal adenocarcinomas, whereas tumors from GW501516-treated animals were adenosquamous and squamous cell carcinomas. Gene expression analysis of tumors arising from GW7845- and GW501516-treated mice identified expression profiles that were distinct from each other and from untreated control tumors of the same histopathology. Only tumors from mice treated with the PPARgamma agonist expressed estrogen receptor-alpha in luminal transit cells, suggesting increased ductal progenitor cell expansion. Tumors from mice treated with the PPARdelta agonist exhibited increased PPARdelta levels and activated 3-phosphoinositide-dependent protein kinase-1 (PDK1), which co-associated, suggesting a link between the known oncogenic activity of PDK1 in mammary epithelium and PPARdelta activation. These results indicate that PPARdelta and PPARgamma agonists produce diverse, yet profound effects on mammary tumorigenesis that give rise to distinctive histopathologic patterns of tumor differentiation and tumor development. |
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| AbstractList | Peroxisome proliferator-activated receptor (PPAR) represents a ligand-dependent nuclear receptor family that regulates multiple metabolic processes associated with fatty acid beta -oxidation, glucose utilization, and cholesterol transport. These and other receptor-mediated actions pertain to their role in hypolipidemic and antidiabetic therapies and as potential targets for cancer chemopreventive agents. The present study evaluated the chemopreventive activity of two highly potent and selective PPAR gamma and PPAR delta agonists in a progestin- and carcinogen-induced mouse mammary tumorigenesis model. Animals treated with the PPAR gamma agonist GW7845 exhibited a moderate delay in tumor formation. In contrast, animals treated with the PPAR delta agonist GW501516 showed accelerated tumor formation. Significantly, tumors from GW7845-treated mice were predominantly ductal adenocarcinomas, whereas tumors from GW501516-treated animals were adenosquamous and squamous cell carcinomas. Gene expression analysis of tumors arising from GW7845- and GW501516-treated mice identified expression profiles that were distinct from each other and from untreated control tumors of the same histopathology. Only tumors from mice treated with the PPAR gamma agonist expressed estrogen receptor- alpha in luminal transit cells, suggesting increased ductal progenitor cell expansion. Tumors from mice treated with the PPAR delta agonist exhibited increased PPAR delta levels and activated 3-phosphoinositide-dependent protein kinase-1 (PDK1), which co-associated, suggesting a link between the known oncogenic activity of PDK1 in mammary epithelium and PPAR delta activation. These results indicate that PPAR delta and PPAR gamma agonists produce diverse, yet profound effects on mammary tumorigenesis that give rise to distinctive histopathologic patterns of tumor differentiation and tumor development. Peroxisome proliferator-activated receptor (PPAR) represents a ligand-dependent nuclear receptor family that regulates multiple metabolic processes associated with fatty acid beta-oxidation, glucose utilization, and cholesterol transport. These and other receptor-mediated actions pertain to their role in hypolipidemic and antidiabetic therapies and as potential targets for cancer chemopreventive agents. The present study evaluated the chemopreventive activity of two highly potent and selective PPARgamma and PPARdelta agonists in a progestin- and carcinogen-induced mouse mammary tumorigenesis model. Animals treated with the PPARgamma agonist GW7845 exhibited a moderate delay in tumor formation. In contrast, animals treated with the PPARdelta agonist GW501516 showed accelerated tumor formation. Significantly, tumors from GW7845-treated mice were predominantly ductal adenocarcinomas, whereas tumors from GW501516-treated animals were adenosquamous and squamous cell carcinomas. Gene expression analysis of tumors arising from GW7845- and GW501516-treated mice identified expression profiles that were distinct from each other and from untreated control tumors of the same histopathology. Only tumors from mice treated with the PPARgamma agonist expressed estrogen receptor-alpha in luminal transit cells, suggesting increased ductal progenitor cell expansion. Tumors from mice treated with the PPARdelta agonist exhibited increased PPARdelta levels and activated 3-phosphoinositide-dependent protein kinase-1 (PDK1), which co-associated, suggesting a link between the known oncogenic activity of PDK1 in mammary epithelium and PPARdelta activation. These results indicate that PPARdelta and PPARgamma agonists produce diverse, yet profound effects on mammary tumorigenesis that give rise to distinctive histopathologic patterns of tumor differentiation and tumor development. Abstract Peroxisome proliferator-activated receptor (PPAR) represents a ligand-dependent nuclear receptor family that regulates multiple metabolic processes associated with fatty acid β-oxidation, glucose utilization, and cholesterol transport. These and other receptor-mediated actions pertain to their role in hypolipidemic and antidiabetic therapies and as potential targets for cancer chemopreventive agents. The present study evaluated the chemopreventive activity of two highly potent and selective PPARγ and PPARδ agonists in a progestin- and carcinogen-induced mouse mammary tumorigenesis model. Animals treated with the PPARγ agonist GW7845 exhibited a moderate delay in tumor formation. In contrast, animals treated with the PPARδ agonist GW501516 showed accelerated tumor formation. Significantly, tumors from GW7845-treated mice were predominantly ductal adenocarcinomas, whereas tumors from GW501516-treated animals were adenosquamous and squamous cell carcinomas. Gene expression analysis of tumors arising from GW7845- and GW501516-treated mice identified expression profiles that were distinct from each other and from untreated control tumors of the same histopathology. Only tumors from mice treated with the PPARγ agonist expressed estrogen receptor-α in luminal transit cells, suggesting increased ductal progenitor cell expansion. Tumors from mice treated with the PPARδ agonist exhibited increased PPARδ levels and activated 3-phosphoinositide–dependent protein kinase-1 (PDK1), which co-associated, suggesting a link between the known oncogenic activity of PDK1 in mammary epithelium and PPARδ activation. These results indicate that PPARδ and PPARγ agonists produce diverse, yet profound effects on mammary tumorigenesis that give rise to distinctive histopathologic patterns of tumor differentiation and tumor development. |
| Author | KOZIKOWSKI, Alan P KOPLEOVICH, Levy DETTIN, Luis E GLAZER, Robert I RUSSELL, Robert G RENKUI BAI WEI, Zhi-Liang YUZHI YIN |
| Author_xml | – sequence: 1 surname: YUZHI YIN fullname: YUZHI YIN organization: Department of Oncology, Georgetown University, Washington, District of Columbia, United States – sequence: 2 givenname: Robert G surname: RUSSELL fullname: RUSSELL, Robert G organization: Department of Oncology, Georgetown University, Washington, District of Columbia, United States – sequence: 3 givenname: Luis E surname: DETTIN fullname: DETTIN, Luis E organization: Department of Oncology, Georgetown University, Washington, District of Columbia, United States – sequence: 4 surname: RENKUI BAI fullname: RENKUI BAI organization: Department of Oncology, Georgetown University, Washington, District of Columbia, United States – sequence: 5 givenname: Zhi-Liang surname: WEI fullname: WEI, Zhi-Liang organization: Department of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, Illinois, United States – sequence: 6 givenname: Alan P surname: KOZIKOWSKI fullname: KOZIKOWSKI, Alan P organization: Department of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, Illinois, United States – sequence: 7 givenname: Levy surname: KOPLEOVICH fullname: KOPLEOVICH, Levy organization: Division of Chemoprevention, National Cancer Institute, Bethesda, Maryland, United States – sequence: 8 givenname: Robert I surname: GLAZER fullname: GLAZER, Robert I organization: Department of Oncology, Georgetown University, Washington, District of Columbia, United States |
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| Keywords | Agonist Toxicity Tumor progression Mammary gland Cell differentiation Differentiation Carcinogenesis Peroxisome proliferator activated receptor |
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| Snippet | Peroxisome proliferator-activated receptor (PPAR) represents a ligand-dependent nuclear receptor family that regulates multiple metabolic processes associated... Abstract Peroxisome proliferator-activated receptor (PPAR) represents a ligand-dependent nuclear receptor family that regulates multiple metabolic processes... |
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| SubjectTerms | Animals Anticarcinogenic Agents - pharmacology Antineoplastic agents Biological and medical sciences Carcinoma, Adenosquamous - chemically induced Carcinoma, Adenosquamous - drug therapy Carcinoma, Adenosquamous - pathology Carcinoma, Adenosquamous - prevention & control Carcinoma, Ductal - chemically induced Carcinoma, Ductal - drug therapy Carcinoma, Ductal - pathology Carcinoma, Ductal - prevention & control Carcinoma, Squamous Cell - chemically induced Carcinoma, Squamous Cell - drug therapy Carcinoma, Squamous Cell - pathology Carcinoma, Squamous Cell - prevention & control Cell Differentiation - drug effects Disease Progression Female Gene Expression Profiling Mammary Neoplasms, Experimental - chemically induced Mammary Neoplasms, Experimental - drug therapy Mammary Neoplasms, Experimental - pathology Mammary Neoplasms, Experimental - prevention & control Medical sciences Mice Oxazoles - pharmacology Pharmacology. Drug treatments PPAR delta - agonists PPAR gamma - agonists Thiazoles - pharmacology Tumors Tyrosine - analogs & derivatives Tyrosine - pharmacology |
| Title | Peroxisome proliferator-activated receptor δ and γ agonists differentially alter tumor differentiation and progression during mammary carcinogenesis |
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