No abstract

No abstract

No abstract

Prostate cancer remains the most prevalent cancer among men worldwide. This cancer is hormone-dependent; therefore, androgen, estrogen, and their receptors play an important role in development and progression of this disease, and in emergence of the castration-resistant prostate cancer (CRPC). Galectins are a family of β-galactoside-binding proteins which are frequently altered (upregulated or downregulated) in a wide range of tumors, participating in different stages of tumor development and progression, but the molecular mechanisms which regulate its expression are still poorly understood. This review provides an overview of the current and emerging knowledge on Galectin-3 in cancer biology with focus on prostate cancer and the interplay with estrogen receptor (ER) signaling pathways, present in androgen-independent prostate cancer cells. We suggest a molecular mechanism where ER, Galectin-3 and β-catenin can modulate nuclear transcriptional events, such as, proliferation, migration, invasion, and anchorage-independent growth of androgen-independent prostate cancer cells. Despite a number of achievements in targeted therapy for prostate cancer, CRPC may eventually develop, therefore new effective drug targets need urgently to be found. Further understanding of the role of Galectin-3 and ER in prostate cancer will enhance our understanding of the molecular mechanisms of prostate cancer development and the future treatment of this disease.

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.