Collagen and prostaglandin E₂ regulate aromatase expression through the PI3K/AKT/IKK and the MAP kinase pathways in adipose stromal cells.
Tan T., Wang L., Wang B.
Laboratory Study, published in Mol Med Rep (2015) — 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
- Mol Med Rep (2015)
- Country
- Greece
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 26059638
- DOI
- 10.3892/mmr.2015.3901
Abstract (original English)
Excessive local estrogen production in the breast promotes estrogen-dependent breast cancer. Aromatase is a key enzyme in estrogen biosynthesis. Aromatase inhibitors used in the treatment of breast cancer are very effective, but indiscriminately reduce estrogen synthesis in all tissues, causing major side‑effects. It is thus desirable to develop inhibitors that selectively block aromatase and estrogen production in breast cancer. To this end, it is important to identify the mechanisms by which aromatase is activated in the tumor microenvironment. Prostaglandin E2 (PGE2) and collagen are two important factors in the tumor microenvironment, which contribute to tumor development and progression. In this study, we show that collagen‑induced aromatase expression in adipose stromal cells (ASCs) was significantly reduced by inhibitors of phosphatidylinositide 3‑kinase (PI3K), IκB kinase (IKK), mitogen‑activated protein kinase kinase (MEK), c‑Jun NH2‑terminal kinase (JNK), protein kinase A (PKA), and by the knockdown of the JunB and AKT2 genes. In addition, PGE2‑induced aromatase expression was significantly inhibited by inhibitors of IKK, MEK, JNK, p38 and PKA. These results indicate that the PI3K/AKT/IKK and the mitogen‑activated protein (MAP) kinase pathways are involved in collagen‑ and PGE2‑induced aromatase expression, and also suggest that collagen and PGE2‑induced signaling pat
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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