ESM-1 siRNA敲低降低前列腺癌细胞中CXCL3的迁移和表达

Juan Rebollo, Jan Geliebter, Niradiz Reyes
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引用次数: 0

摘要

内皮细胞特异性分子-1 (Endothelial cell-specific molecule-1, ESM-1),也被称为内啡肽,是一种由血管内皮表达的可溶性蛋白多糖,也在血液中循环。炎症细胞因子和促血管生成生长因子增加其表达,并且在几种癌症类型和免疫功能正常的败血症患者中已报道血清水平升高。本研究的目的是分析cxc趋化因子的表达谱,以及ESM-1基因敲低对高转移性人前列腺PC-3细胞增殖、迁移和cxc趋化因子表达的影响。分析了转移性PC-3和非致瘤性PWR-1E细胞中cxc趋化因子的表达谱。在PC-3细胞中进行了sirna介导的ESM-1敲低,随后测试了细胞迁移和增殖。在转录物和蛋白水平进一步量化siRNA转染对cxc趋化因子表达的影响。RT-qPCR分析和夹心ELISA分析显示,与非致瘤性PWR-1E相比,转移性PC-3细胞中ESM-1和几种cxc趋化因子的水平更高。用ESM-1-siRNA转染PC-3细胞可减少细胞迁移,但不影响细胞增殖,并伴有血管生成趋化因子CXCL3转录物和蛋白水平的降低。我们在这里首次报道了ESM-1靶向PC-3细胞,导致迁移减少,这可能与血管生成CXCL3趋化因子的表达减少有关,至少部分与ESM-1- sirna转染细胞中CXCL3趋化因子的表达减少有关。需要进一步的研究来确定ESM-1在前列腺癌细胞中的生物学作用以及与CXCL3表达的联系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

ESM-1 siRNA Knockdown Decreased Migration and Expression of CXCL3 in Prostate Cancer Cells.

ESM-1 siRNA Knockdown Decreased Migration and Expression of CXCL3 in Prostate Cancer Cells.

ESM-1 siRNA Knockdown Decreased Migration and Expression of CXCL3 in Prostate Cancer Cells.

ESM-1 siRNA Knockdown Decreased Migration and Expression of CXCL3 in Prostate Cancer Cells.

Endothelial cell-specific molecule-1 (ESM-1), also known as endocan, is a soluble proteoglycan expressed by the vascular endothelium, which also circulates in the bloodstream. Inflammatory cytokines and proangiogenic growth factors increase its expression, and increased serum levels have been reported in several cancer types and immunocompetent patients with sepsis. The aim of this study was to analyze the expression profile of CXC-chemokines and the effects of ESM-1 gene knockdown in proliferation, migration and CXC-chemokine expression in highly metastatic human prostate PC-3 cells. Expression profiles of CXC-chemokines were analyzed in metastatic PC-3 and non-tumorigenic PWR-1E cells. siRNA-mediated knockdown of ESM-1 was performed into PC-3 cells, which were subsequently tested for cell migration and proliferation. Effect of siRNA transfection on CXC-chemokine expression was further quantified at the transcript and protein level. RT-qPCR analysis and sandwich ELISA assay revealed higher levels of ESM-1 and several CXC-chemokines in metastatic PC-3 cells compared to non-tumorigenic PWR-1E. Transfection of PC-3 cells with ESM-1-siRNA decreased cell migration with no effect on proliferation, and it was accompanied by decrease in the transcript and protein levels of the angiogenic chemokine CXCL3. We report here for the first time the ESM-1 targeting in PC-3 cells, which resulted in decreased migration, which may be related, at least in part, to decreased expression of the angiogenic CXCL3 chemokine, whose expression was found to be reduced in ESM-1-siRNA transfected cells. Additional studies are required to ascertain the biological role of ESM-1 in prostate cancer cells and the link with the expression of CXCL3.

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