Open AccessEstradiol–estrogen receptor: A key interplay of the expression of syndecan‐2 and metalloproteinase‐9 in breast cancer cells
Author(s) -
Kousidou Olga Ch.,
Berdiaki Aikaterini,
Kletsas Dimitris,
Zafiropoulos Alexandros,
Theocharis Achilleas D.,
Tzanakakis George N.,
Karamanos Nikos K.
Publication year - 2008
Publication title -
molecular oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.332
H-Index - 88
eISSN - 1878-0261
pISSN - 1574-7891
DOI - 10.1016/j.molonc.2008.06.002
Subject(s) - estrogen receptor , breast cancer , metalloproteinase , cancer research , estrogen , estrogen receptor beta , syndecan 1 , receptor , estrogen receptor alpha , biology , cancer , medicine , microbiology and biotechnology , matrix metalloproteinase , endocrinology , biochemistry , cell
Estrogens are related with the growth and development of target tissues and play a critical role in breast cancer progression. The effects of estrogens are mediated by the estrogen receptors ERα and ERβ, which are members of the nuclear steroid receptor superfamily. To date, it is not known how these hormones elicit many of their effects on extracellular matrix molecules and how these effects can be connected with ER expression. For this purpose, the effect of estradiol on ER expression as well as on proteoglycan and metalloproteinase expression was studied. The effect of E2 on extracellular matrix molecule expression has been studied using ERα suppression in breast cancer cells. Our studies using ERα‐positive MCF‐7 cells show that estradiol affects the expression of syndecan‐2, but not of syndecan‐4, through ERα. Furthermore, the ability of estradiol to affect MMP‐9 and TIMP‐1 expression is connected with ERα status. Together, these data demonstrate the significant role of ERα on mediating the effect of estradiol on extracellular matrix molecules.