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Overexpression of Glypican 5 (GPC5) Inhibits Prostate Cancer Cell Proliferation and Invasion via Suppressing Sp1-Mediated EMT and Activation of Wnt/beta-Catenin Signaling

机译:甘醇5(GPC5)的过度表达抑制前列腺癌细胞增殖和侵袭通过抑制SP1介导的EMT和WNT /β-连环蛋白信号传导的活化

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摘要

Glypican 5 (GPC5) belongs to the family of heparan sulfate proteoglycans (HSPGs). It was initially known as a regulator of growth factors and morphogens. Recently, there have been reports on its correlation with the tum-origenic process in the development of some cancers. However, little is known about its precise role in prostate cancer (PCa). In the present study, we explored the expression pattern and biological functions of GPC5 in PCa cells. Our results showed that GPC5 was lowly expressed in PCa cell lines. Upregulation of GPC5 significantly inhibited PCa cell proliferation and invasion in vitro as well as attenuated tumor growth in vivo. We also found that overexpression of GPC5 inhibited the epithelial-mesenchymal transition (EMT) and Wnt/beta-catenin signaling activation, which was mediated by Sp1. Taken together, we suggest GPC5 as a tumor suppressor in PCa and provide promising therapeutic strategies for PCa.
机译:甘醇5(GPC5)属于硫酸乙酰肝素蛋白多糖(HSPG)的家族。 它最初被称为生长因子和形态的调节剂。 最近,已经报告了与某些癌症发育中的北常心过程的相关性。 然而,对前列腺癌(PCA)中的其精确作用知之甚少。 在本研究中,我们探讨了GPC5在PCA细胞中的表达模式和生物学功能。 我们的研究结果表明,GPC5在PCA细胞系中略低。 GPC5的上调显着抑制了体外的PCA细胞增殖和侵袭,以及体内减毒的肿瘤生长。 我们还发现GPC5的过表达抑制了由SP1介导的上皮 - 间充质转换(EMT)和WNT /β-连环蛋白信号激活。 一起服用,我们建议GPC5作为PCA的肿瘤抑制器,并为PCA提供了有希望的治疗策略。

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