Epigenetic mechanisms regulate the prostaglandin E receptor 2 in breast cancer.

摘要: The increase in local oestrogen production seen receptor positive (ER+) breast cancers is driven by increased activity of the aromatase enzyme. CYP19A1, encoding gene for aromatase, often overexpressed oestrogen-producing cells adipose fibroblasts (BAFs) surrounding an ER+ tumour, and molecular processes underlying this upregulation important development breast-specific inhibitors cancer therapy. Prostaglandin E2 (PGE2), a factor secreted tumours, known to stimulate CYP19A1 expression human BAFs. hormonal regulation process has been examined; however, what less well understood emerging role epigenetic mechanisms how they modulate PGE2 signalling. This present study characterises prostanoid EP2 context cancer. Sodium bisulphite sequencing CpG methylation within promoter region revealed that inverse correlation existed between levels relative cell lines MDA-MB-231, MCF7 MCF10A but not HS578t T47D. Inhibition DNA with 5-aza-2'-deoxycytidine (5aza) histone deacetylation Trichostatin A (TSA) resulted mRNA all varying influences each observed. Expression was detected BAFs despite natively methylated promoter, further upon 5aza treatment. An examination 3 triple negative, ductal carcinoma situ invasive samples there no change status normal associated stroma, observed differences levels. Although inversely correlated established lines, we could identify such tumour-associated stroma cells.