15-Deoxy-Δ12,14-prostaglandin J2-induced apoptosis does not require PPARγ in breast cancer cells
Open accessAbstract
Naturally occurring derivatives of arachidonic acid are potent agonists for the nuclear hormone receptor peroxisome proliferator-activated receptor gamma (PPARgamma) and block cancer cell proliferation through the induction of apoptosis. We have previously reported that induction of apoptosis using cyclopentenone prostaglandins of the J series, including 15deoxydelta(12,14)PGJ(2) (15dPGJ(2)), is associated with a high degree of PPAR-response element (PPRE) activity and requires early de novo gene expression in breast cancer cells. In the current study, we used pharmacologic and genetic approaches to test the hypothesis that PPARgamma is required for 15dPGJ(2)-induced apoptosis. The PPARgamma agonists 15dPGJ(2), trogliltazone (TGZ), and GW7845, a synthetic and highly selective tyrosine-based PPARgamma agonist, all increased transcriptional activity of PPARgamma, and expression of CD36, a PPARgamma-dependent gene. Transcriptional activity and CD36 expression was reduced by GW9662, a selective and irreversible PPARgamma antagonist, but GW9662 did not block apoptosis induced by 15dPGJ(2). Moreover, dominant negative expression of PPARgamma blocked PPRE transcriptional activity, but did not block 15dPGJ(2)-induced apoptosis. These studies show that while 15dPGJ(2) activates PPRE-mediated transcription, PPARgamma is not required for 15dPGJ(2)-induced apoptosis in breast cancer cells. Other likely mechanisms through which cyclopentenone prostaglandins induce apoptosis of cancer cells are discussed.
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Recent in vitro studies indicate that the effects of PPARγ agonists on cell growth are often independent of the presence of PPARγ, so the clinical relevance of in vitro findings is unclear.
“However, since recent in vitro studies indicate that the effects of PPARγ agonists on cell growth are often independent of the presence of PPARγ (100–102), the clinical relevance of findings of in vitro studies is unclear.”
From Diabetes and Cancer (2010) · cites this paper as [101]
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- Authors
- Clay, C. E., Monjazeb, A., Thorburn, J., Chilton, F. H., & High, K. P.
- Affiliations
- Atrium Health Wake Forest Baptist (US)
- Corresponding author
- High, Kevin P.
- Venue
- Journal of Lipid Research
- Publisher
- Elsevier BV
- Published
- 2002-11
- Volume
- 43
- Issue
- 11
- Pages
- 1818-1828
- ISSN
- 0022-2275 (ISSN-L)
- OpenAlex
- W2184417866
- Cited by
- 103
- References
- 81
- Citations by year
- 2022: 1 · 2021: 3 · 2020: 1 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 2 · 2014: 3 · 2013: 4 · 2012: 2
- FWCI
- 3.25
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Lipid Research (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (1r01ai042022-01a1, CA‐12197)
- U.S. Army
- National Cancer Institute (CA12197-27, P30CA012197)
- National Institute of Allergy and Infectious Diseases (R01 AI 42022)
- U.S. Army Medical Research Acquisition Activity
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Keywords
- 15-deoxy-Δ12,14-prostaglandin J2, cyclopentenone prostaglandins, PPARγ, apoptosis, breast cancer cells, PPAR response element, CD36, GW9662, troglitazone
- MeSH terms
- Breast Neoplasms, Cell Nucleus, Fluorescent Antibody Technique, Time Factors, Transcription Factors, Transcription, Genetic, Tumor Cells, Cultured, Prostaglandin D2, Gene Expression Regulation, Neoplastic, Apoptosis, Receptors, Cytoplasmic and Nuclear, Response Elements, Protein Transport
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Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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