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microRNA-218 inhibits prostate cancer cell growth and promotes apoptosis by repressing TPD52 expression

机译:microRNA-218通过抑制TPD52表达来抑制前列腺癌细胞的生长并促进细胞凋亡

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摘要

The tumor protein D52 (TPD52) is an oncogene overexpressed in prostate cancer (PC) due to gene amplification. Although the oncogenic effect of TPD52 is well recognized, how its expression is regulated is still not clear. This study tried to explore the regulative role of miR-218, a tumor suppressing miRNA on TPD52 expression and prostate cancer cell proliferation. We found the expression of miR-218 was significantly lower in PC specimens. Based on gain and loss of function analysis, we found miR-218 significantly inhibit cancer cell proliferation by inducing apoptosis. These results strongly suggest that miR-218 plays a tumor suppressor role in PC cells. In addition, our data firstly demonstrated that miR-218 directly regulates oncogenic TPD52 in PC3 cells and the miR-218-TPD52 axis can regulate growth of this prostate cancer cell line. Knockdown of TPD52 resulted in significantly increased cancer cell apoptosis. Clearly understanding of oncogenic TPD52 pathways regulated by miR-218 might be helpful to reveal new therapeutic targets for PC. (C) 2014 Elsevier Inc. All rights reserved.
机译:肿瘤蛋白D52(TPD52)是由于基因扩增而在前列腺癌(PC)中过表达的癌基因。尽管TPD52的致癌作用已得到公认,但如何调节其表达仍不清楚。这项研究试图探索miR-218(一种抑制miRNA的肿瘤对TPD52表达和前列腺癌细胞增殖的调节作用)。我们发现miR-218的表达在PC标本中显着降低。基于功能获得和丧失的分析,我们发现miR-218通过诱导凋亡显着抑制癌细胞增殖。这些结果强烈表明,miR-218在PC细胞中起肿瘤抑制作用。另外,我们的数据首先证明,miR-218直接调节PC3细胞中的致癌TPD52,而miR-218-TPD52轴可以调节该前列腺癌细胞系的生长。击倒TPD52导致癌细胞凋亡明显增加。清楚了解miR-218调控的致癌TPD52途径可能有助于揭示PC的新治疗靶标。 (C)2014 Elsevier Inc.保留所有权利。

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