Acceleration of invasive activity via matrix metalloproteinases by transfection of the estrogen receptor-α gene in endometrial carcinoma cells

It is well known that the functions of reproductive organs are regulated by sex steroids and their receptors and it is hypothesized that the progression of neoplasms that originate from the reproductive organs is influenced by them. However, the correlation between sex steroids and tumor progression, especially tumor invasion, is not well known in endometrial carcinoma. In our study, we focused on the influence of estrogen and its receptor in invasion and matrix metalloproteinases (MMI's), which are known to be important in tumor invasion, as well as on endometrial carcinoma cells. The growth of Ishikawa, cells, to which an estrogen receptor-alpha expressing vector was transfected, was accelerated by 17beta-estradiol as was the acceleration of the expression of cyclin D1. By invasion assay, in conditions with 17beta-estradiol, the invasiveness of Ishikawa cells was enhanced. Furthermore, according to the accelerated invasiveness, the expression of MMP-1, -7 and -9 and Ets-1 was enhanced. These results suggest that activation of ER-alpha by estrogen results in tumor progression by stimulating cell growth and invasiveness via acceleration of the expression of MMPs. (C) 2002 Wiley-Liss, Inc.