Estrogen stimulates transcription from the human prolactin distal promoter through AP1 and estrogen responsive elements in T47D human breast cancer cells.

摘要: Abstract Human prolactin (hPRL) is a pleiotropic and versatile hormone that exercises more than 300 biological activities through binding to its cognate receptors. Recently, multiple studies have implicated hPRL in the development of human breast cancer. As target hPRL, both normal neoplastic cells also synthesize secrete which therefore establishes an autocrine/paracrine action loop mammary gland. In contrast extensive regulation expression pituitary gland, tissue cancer has not been extensively addressed. Extrapituitary PRL primarily regulated by distal promoter located 5.8 kb upstream promoter. result alternative usage, extrapituitary different signalling pathways hormones, cytokines or neuropeptides compared pituitary. Here, we present evidence shows estrogen directly induces gene T47D cells. We identified functional, non-canonical responsive element (ERE) AP1 site Gel shift chromatin immunoprecipitation assays demonstrated receptor (ER)α ERβ bind ERE. However, only ERα interacts with proteins Promoter–reporter demonstrate ERE sites are required for full induction activity estradiol. Our suggest interactions between estrogens, ERs, transcription factors may be critical oncogenesis contribute progression