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首页> 外文期刊>International Journal of Molecular Sciences >MicroRNA-331-3p Suppresses Cervical Cancer Cell Proliferation and E6/E7 Expression by Targeting NRP2
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MicroRNA-331-3p Suppresses Cervical Cancer Cell Proliferation and E6/E7 Expression by Targeting NRP2

机译：MicroRNA-331-3p通过靶向NRP2抑制宫颈癌细胞的增殖和E6 / E7表达

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Aberrant expression of microRNAs (miRNAs) is involved in the development and progression of various types of cancers. In this study, we investigated the role of miR-331-3p in cell proliferation and the expression of keratinocyte differentiation markers of uterine cervical cancer cells. Moreover, we evaluated whether neuropilin 2 (NRP2) are putative target molecules that regulate the human papillomavirus (HPV) related oncoproteins E6 and E7. Cell proliferation in the human cervical cancer cell lines SKG-II, HCS-2, and HeLa was assessed using the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2 H -tetrazolium, inner salt (MTS) assay. Cellular apoptosis was measured using the TdT-mediated dUTP nick end labeling (TUNEL) and Annexin V assays. Quantitative RT-PCR was used to measure the messenger RNA (mRNA) expression of the NRP2, E6, E7, p63, and involucrin (IVL) genes. A functional assay for cell growth was performed using cell cycle analyses. Overexpression of miR-331-3p inhibited cell proliferation, and induced G2/M phase arrest and apoptosis in SKG-II, HCS-2 and HeLa cells. The luciferase reporter assay of the NRP2 3′-untranslated region revealed the direct regulation of NRP2 by miR-331-3p. Gene expression analyses using quantitative RT-PCR in SKG-II, HCS-2, and HeLa cells overexpressing miR-331-3p or suppressing NRP2 revealed down-regulation of E6, E7, and p63 mRNA and up-regulation of IVL mRNA. Moreover, miR-331-3p overexpression was suppressed NRP2 expression in protein level. We showed that miR-331-3p and NRP2 were key effectors of cell proliferation by regulating the cell cycle, apoptosis. NRP-2 also regulates the expression of E6/E7 and keratinocyte differentiation markers. Our findings suggest that miR-331-3p has an important role in regulating cervical cancer cell proliferation, and that miR-331-3p may contribute to keratinocyte differentiation through NRP2 suppression. miR-331-3p and NRP2 may contribute to anti-cancer effects.
机译：microRNA（miRNA）的异常表达与各种类型的癌症的发生和发展有关。在这项研究中，我们调查了miR-331-3p在子宫宫颈癌细胞的细胞增殖和角质形成细胞分化标志物的表达中的作用。此外，我们评估了神经pilin 2（NRP2）是否是调节人类乳头瘤病毒（HPV）相关癌蛋白E6和E7的假定靶分子。使用3-（4,5-二甲基噻唑-2-基）-5-（3-羧基甲氧基苯基）-2-（4-）评估人宫颈癌细胞SKG-II，HCS-2和HeLa中的细胞增殖磺基苯基）-2 H-四唑鎓，内盐（MTS）分析。使用TdT介导的dUTP缺口末端标记（TUNEL）和膜联蛋白V测定法测量细胞凋亡。定量RT-PCR用于测量NRP2，E6，E7，p63和involucrin（IVL）基因的信使RNA（mRNA）表达。使用细胞周期分析进行细胞生长的功能测定。 miR-331-3p的过表达抑制细胞增殖，并诱导SKG-II，HCS-2和HeLa细胞中G2 / M期阻滞和凋亡。 NRP2 3'-非翻译区的荧光素酶报告基因测定揭示了miR-331-3p对NRP2的直接调节。在过量表达miR-331-3p或抑制NRP2的SKG-II，HCS-2和HeLa细胞中使用定量RT-PCR进行基因表达分析，结果显示E6，E7和p63 mRNA的下调和IVL mRNA的上调。此外，miR-331-3p过表达在蛋白水平上抑制了NRP2表达。我们显示，miR-331-3p和NRP2通过调节细胞周期和凋亡是细胞增殖的关键效应器。 NRP-2还调节E6 / E7和角质形成细胞分化标记的表达。我们的发现表明，miR-331-3p在调节宫颈癌细胞增殖中具有重要作用，而miR-331-3p可能通过抑制NRP2促进角质形成细胞分化。 miR-331-3p和NRP2可能有助于抗癌作用。

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