The expression and correlation between the transcription factor FOXP1 and estrogen receptors in epithelial ovarian cancer

Background: Estrogen plays an important role in the progression of ovarian cancer in humans. FOXP1 belongs to the forkhead/winged-helix transcription factor family, and previous research indicated that FOXP1 functioned as a tumor suppressor gene. FOXP1 may be similar to FOXA1 and is closely related to steroid hormone receptors, but the relationship between FOXP1 and ER currently remains unclear. Methods: Ovarian tumors (60 malignant cases, 26 borderline cases, and 13 benign cases) and 14 normal ovarian tissues were collected retrospectively. Immunohistochemistry, western blotting and real-time PCR were used to characterize the expression patterns of FOXP1, ER alpha, and ER beta both at the mRNA and protein levels. We also used co-immunoprecipitation and immunofluorescent colocalization to investigate whether a correlation exists between FOXP1 and ER alpha/ER beta in ovarian cancer tissues. Results: The mRNA level for FOXP1 and ER beta in ovarian carcinoma tissues decreased, while the expression level of ER alpha mRNA increased compared with normal ovarian tissues. With an increase in the degree of ovarian carcinoma malignancy, the ER alpha expression level also increased. The expression pattern of ER beta in ovarian neoplasms was similar to that of the FOXP1 protein; presenting nuclear staining decreased, while cytoplasmic expression increased. Colocalization of FOXP1, ER alpha, and ER beta was present in the cytoplasm, with ER beta specific co-localization with FOXP1 in the perinuclear area. While immunoprecipitates created with FOXP1 mouse anti-human monoclonal antibody showed a positive reaction to an anti-ER antibody, irnmunoprecipitates containing anti-ER antibody and react to anti-FOXP1 antibody. Conclusion: Interactions between FOXP1 and ER may play a pivotal role in the progression of ovarian cancer, and the activation or induction of FOXP1 and ER beta expression in cancer cells may inhibit tumor proliferation. (C) 2014 Elsevier B.V. and Societe francaise de biochimie et biologie Moleculaire (SFBBM). All rights reserved.