Prostaglandin E2 regulates aromatase activity and expression in human adipose stromal cells via two distinct receptor subtypes.
Richards JA., Brueggemeier RW.
Laboratory Study, published in J Clin Endocrinol Metab (2003) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- J Clin Endocrinol Metab (2003)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 12788892
- DOI
- 10.1210/jc.2002-021475
Abstract (original English)
The aromatase enzyme complex, located primarily in the stromal cells of breast tumors, catalyzes estrogen biosynthesis and is fundamental to hormone-dependent growth of breast cancer. Although an important pharmacological target, the mechanisms by which aromatase is regulated are poorly understood. Thus, regulation of aromatase activity and expression in human breast stromal cells by prostaglandin E(2) (PGE(2)) was investigated. PGE(2) exerts its actions via four transmembrane receptors, EP(1), EP(2), EP(3), and EP(4), which coordinate different signal transduction pathways. Using selective receptor agonists and antagonists, the involvement of the EP(1), EP(2), and EP(3) subtypes was assessed. Enzyme activity levels in cultures of disease-free stromal cells were determined using a tritiated water-release assay. PGE(2) and agonists of EP(1) and EP(2) significantly increased aromatase activity levels, which were decreased by the corresponding antagonists. An agonist of EP(3), an inhibitory pathway, antagonized activity levels induced by PGE(2). These results were generally reflective of changes in aromatase protein expression, determined by Western blotting analysis and the pattern of mRNA expression determined by a competitive RT-PCR method. Collectively, the results demonstrate that regulation of aromatase by PGE(2) is complex and may influence the development and progression o
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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