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首页> 外文期刊>Journal of cellular biochemistry. >MicroRNA-182 promotes cell growth, invasion, and chemoresistance by targeting programmed cell death 4 (PDCD4) in human ovarian carcinomas
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MicroRNA-182 promotes cell growth, invasion, and chemoresistance by targeting programmed cell death 4 (PDCD4) in human ovarian carcinomas

机译：MicroRNA-182通过靶向人卵巢癌中的程序性细胞死亡4（PDCD4）促进细胞生长，侵袭和化学抗性

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摘要

As an important tumor suppressor, programmed cell death 4 (PDCD4) influences transcription and translation of multiple genes, and modulates different signal transduction pathways. However, the upstream regulation of this gene is largely unknown. In this study, we found that microRNA-182 (miRNA-182, miR-182) was upregulated, whereas PDCD4 was downregulated in ovarian cancer tissues and cell lines. Blocking or increase of miR-182 in ovarian cancer cell lines led to an opposite alteration of endogenous PDCD4 protein level. Using fluorescent reporter assay, we confirmed the direct and negative regulation of PDCD4 by miR-182, which was dependent on the predicted miR-182 binding site within PDCD4 3′ untranslated region (3′ UTR). MTT and colony formation assays suggested that miR-182 blockage suppressed, whereas miR-182 mimics enhanced viability and colony formation of ovarian cancer cells. These effects may partly be attributed to the cell cycle promotion activity of miR-182. miR-182 also contributed to migration and invasion activities of ovarian cancer cells. Furthermore, miR-182 reduced the chemosensitivity of ovarian cancer cells to CDDP and Taxol, possibly by its anti-apoptosis activity. Importantly, all the alterations of the above cellular phenotypes by blocking or enhancing of miR-182 could be alleviated by subsequent suppression or ectopic expression of its target PDCD4, respectively. We conclude that in ovarian cancer cells, miR-182 acts as an oncogenic miRNA by directly and negatively regulating PDCD4.
机译：作为重要的肿瘤抑制因子，程序性细胞死亡4（PDCD4）影响多个基因的转录和翻译，并调节不同的信号转导途径。但是，该基因的上游调控在很大程度上是未知的。在这项研究中，我们发现在卵巢癌组织和细胞系中，microRNA-182（miRNA-182，miR-182）被上调，而PDCD4被下调。卵巢癌细胞系中miR-182的阻滞或增加导致内源性PDCD4蛋白水平发生相反的变化。使用荧光报告基因检测，我们证实了miR-182对PDCD4的直接和负调控，这取决于PDCD4 3'非翻译区（3'UTR）中预测的miR-182结合位点。 MTT和集落形成试验表明，miR-182阻滞被抑制，而miR-182模仿物增强了卵巢癌细胞的活力和集落形成。这些作用可能部分归因于miR-182的细胞周期促进活性。 miR-182还有助于卵巢癌细胞的迁移和侵袭活动。此外，miR-182可能通过其抗凋亡活性降低了卵巢癌细胞对CDDP和紫杉醇的化学敏感性。重要的是，通过阻断或增强miR-182，上述细胞表型的所有改变可以分别通过其靶PDCD4的随后抑制或异位表达来缓解。我们得出的结论是，在卵巢癌细胞中，miR-182通过直接和负调控PDCD4充当致癌miRNA。

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