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Epigallocatechin-3-gallate reduces the proliferation of benign prostatic hyperplasia cells via regulation of focal adhesions

机译：Epigallocatechin-3-gallate通过调节局灶性粘连来减少良性前列腺增生细胞的增殖

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Abstract Aims Benign prostatic hyperplasia (BPH) is the most common urological disease that is characterized by the excessive growth of prostatic epithelial and stromal cells. Pharmacological therapy for BPH has limited use due to the many side effects so there is a need for new agents including natural compounds such as epigallocatechin-3-gallate (EGCG). This study was undertaken to assess the role of EGCG, suppressing the formation of BPH by reducing inflammation and oxidative stress, in cytoskeleton organization and ECM interactions via focal adhesions. Main methods We performed MTT assay to investigate cell viability of BPH-1 cells, wound healing assay to examine cell migration, immunofluorescence assay for F-actin organization and paxillin distribution and finally immunoblotting to investigate focal adhesion protein levels in the presence and absence of EGCG. Key findings We found that EGCG inhibits cell proliferation at the concentration of 89.12μM, 21.2μM and 2.39μM for 24, 48 and 72h, respectively as well as inhibitory effects of EGCG on BPH-1 cell migration were observed in a wound healing assay. Furthermore, it was determined by immunofluorescence labeling that EGCG disrupts F-actin organization and reduces paxillin distribution. Additionally, EGCG decreases the activation of FAK (Focal Adhesion Kinase) and the levels of paxillin, RhoA (Ras homolog gene family, member A), Cdc42 (cell division cycle 42) and PAK1 (p21 protein-activated kinase 1) in a dose-dependent manner. Significance For the first time, by this study, we found evidence that BPH-1 cell proliferation could be inhibited with EGCG through the disruption of cytoskeleton organization and ECM interactions. Consequently, EGCG might be useful in the prevention and treatment of diseases characterized by excessive cell proliferation such as BPH.
机译：摘要目的良性前列腺增生（BPH）是最常见的泌尿病，其特征在于前列腺上皮和基质细胞的过度生长。由于许多副作用，BPH的药理治疗有限的使用，因此需要新的药剂，包括天然化合物，例如EpigallocateChin-3-gallate（EGCG）。本研究旨在评估EGCG的作用，通过降低炎症和氧化应激，通过局部粘连降低炎症和氧化应激来抑制BPH的形成。主要方法我们进行了MTT测定以研究BPH-1细胞的细胞活力，伤口愈合测定检查细胞迁移，用于F-肌动蛋白组织的免疫荧光测定和Paxillin分布以及最终免疫印迹，以研究eGCG存在和不存在的局灶性粘附蛋白水平。主要发现我们发现EGCG抑制浓度为89.12μm，21.2μm和2.39μm的细胞增殖以及21,48和72h的浓度，以及EGCG对BPH-1细胞迁移的抑制作用在伤口愈合测定中观察到。此外，通过免疫荧光标记来确定EGCG破坏F-肌动蛋白组织并减少百素分布。另外，EGCG降低了FAK（焦点粘附激酶）的激活和百叶蛋白，rhOA（RAS同源物基因家族，成员A），CDC42（细胞分裂周期42）和PAK1（P21蛋白激活激酶1）的剂量 - 依赖的方式。本研究首次意义，我们发现证据表明，通过破坏细胞骨架组织和ECM相互作用，可以抑制BPH-1细胞增殖。因此，EGCG可用于预防和治疗以诸如BPH的过量细胞增殖的疾病。

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