Premium
Study of the activity of Estrogen Response Elements present on Pax‐5 promoter and their potential role on regulating Pax‐5 expression in breast cancer
Author(s) -
Faye Mame Daro,
Ouellette Rodney
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.lb278
Subject(s) - estrogen receptor , cancer research , estrogen , transcription factor , carcinogenesis , breast cancer , biology , receptor , estrogen receptor beta , oncogene , reporter gene , gper , cancer , gene expression , endocrinology , gene , cell cycle , genetics
Pax‐5 is a transcription factor playing a crucial role in B lymphopoïesis and its deregulation has been associated to certain malignancies, namely non‐Hodgkin lymphomas and acute lymphoblastic leukemia. Although Pax‐5 is mainly known to be expressed in B cells, there is a body of preliminary data generated in our laboratory suggesting its expression in some breast cancer cell lines and primary breast tumors. In an attempt to explain Pax‐5 expression in these breast cancer cases, we analyzed its promoter and found a number of Estrogen Receptor Elements (EREs) and Estrogen Related Receptors sites (ERRs), suggesting a role for estrogen receptors in Pax‐5 expression in breast cancer. Therefore, electrophoretic mobility shift assays (EMSA) were performed to assess the binding capacity of estrogen receptors ERα and ERβ on those predicted sites, which were also cloned in the Luciferase reporter vector pGL3‐Promoter to evaluate the receptors activity by dual luciferase reporter assays. We report here the specific binding of estrogen receptors on some of the EREs located on Pax‐5 promoter and their differential activation under 17β‐estradiol stimulation in MCF‐7 cells. These results suggest a role for estrogen receptors in the expression of the oncogene Pax‐5 in breast cancer and suggest a mechanism that contributes to breast carcinogenesis. This work has been supported by an ''Atlantic Innovation Fund'' grant.