Estrogen receptors regulate galectin‑3 in androgen‑independent DU‑145 prostate cancer cells

Abstract

The aim of the present study was to investigate the role of estrogen receptor (ER)α and ERβ, and galectin-3 (GAL-3) in migration and invasion of androgen-independent DU-145 prostate cancer cells, and to examine the regulation of the expression of GAL-3 by the activation of these receptors. Wound healing and cell invasion assays were performed using the control (basal level of cellular function) and treated DU-145 cells. At 24 h of treatment, 17β-estradiol (E2), the ERα-selective agonist, 4,4' ,4"-(4-propyl-(1H)-pyrazo le-1,3,5-triyl)trisphenol (PPT), or the ERβ-selective agonist, 2,3-bis(4-hydroxyphenyl)-propionitrile (diarylprepionitrile; DPN), increased the migration and invasion of the DU-145 cells. Pre-treatment with the ERα-and ERβ-selective antagonists blocked these effects, indicating that ERα and ERβ are upstream receptors regulating these processes. Western blot analysis and immunofluorescence staining for the detection of the GAL-3 were performed using the control and treated DU-145 cells. Treatment of the DU-145 cells with E2, PPT or DPN for 24 h increased the expression of the GAL-3 compared to the control. Furthermore, a specific inhibitor of GAL-3 (VA03) inhibited the migration and invasion of DU-145 cells, indicating the involvement of the complex ERα/GAL-3 and ERβ/GAL-3 in the regulation of these processes. On the whole, the present study demonstrates that the activation of both ERs increases the expression and signaling of GAL-3, and promotes the migration and invasion of DU-145 cells. The findings of the present study provide novel insight into the signatures and molecular mechanisms of ERα and ERβ in DU-145 cells.