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)‑pyrazole‑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.
摘要：
本研究的目的是探讨雌激素受体（ER）α和ERβ的作用。和半乳糖凝集素-3（GAL-3）在雄激素非依赖性DU-145前列腺癌细胞的迁移和侵袭中，并检查这些受体激活对GAL‑3表达的调节。使用对照(细胞功能的基础水平)和处理的DU‑145细胞进行伤口愈合和细胞侵袭测定。在24小时的治疗，17β-雌二醇（E2），ERα选择性激动剂，4,4\'，4“-(4-丙基-(1H)-吡唑-1,3,5-三基)三苯酚(PPT),或ERβ选择性激动剂，2,3‑双(4‑羟基苯基)‑丙腈(二芳基丙腈;DPN),增加了DU-145细胞的迁移和侵袭。ERα和ERβ选择性拮抗剂的预处理阻断了这些作用，表明ERα和ERβ是调节这些过程的上游受体。使用对照和处理的DU‑145细胞进行用于检测GAL‑3的蛋白质印迹分析和免疫荧光染色。与对照组相比，用E2，PPT或DPN处理DU-145细胞24小时可增加GAL-3的表达。此外，GAL-3的特异性抑制剂（VA03）抑制DU-145细胞的迁移和侵袭，表明复杂的ERα/GAL‑3和ERβ/GAL‑3参与这些过程的调节。总的来说,本研究表明，两种ER的激活都会增加GAL‑3的表达和信号传导，并促进DU‑145细胞的迁移和侵袭。本研究的发现为DU-145细胞中ERα和ERβ的特征和分子机制提供了新的见解。
