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miR-142-3p Suppresses Cell Growth by Targeting CDK4 in Colorectal Cancer

机译：miR-142-3p通过靶向大肠癌中的CDK4抑制细胞生长

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Background/Aims Deregulation of microRNAs (miRNAs) has been associated with a variety of cancers, including colorectal cancer (CRC). Here, we investigated anomalous miR-142-3p expression and its possible functional consequences in primary CRC samples. Methods The expression of miR-142-3p was measured by quantitative RT-PCR in 116 primary CRC tissues and adjacent non-tumor tissues. The effect of miR-142-3p up- or down-regulation in CRC-derived cells was evaluated in vitro by cell viability and colony formation assays and in vivo by growth assays in xenografted nude mice. Results Using quantitative RT-PCR, we found that miR-142-3p was down-regulated in 78.4 % (91/116) of the primary CRC tissues tested when compared to the adjacent non-tumor tissues. We also found that the miR-142-3p mimic reduced in vitro cell viability and colony formation by inducing cell cycle arrest in CRC-derived cells, and inhibited in vivo tumor cell growth in xenografted nude mice. Inversely, we found that the miR-142-3p inhibitor increased the viability and colony forming capacity of CRC-derived cells and tumor cell growth in xenografted nude mice. In addition, we identified CDK4 as a potential target of miR-142-3p by predictions and dual-luciferase reporter assays. Concordantly, we found that miR-142-3p mimics and inhibitors could decrease and increase CDK4 protein levels in CRC-derived cells, respectively. Conclusion From our results we conclude that miR-142-3p may act as a tumor suppressor in CRC and may serve as a tool for miRNA-based CRC therapy.
机译：背景/目的microRNA（miRNA）的失调与多种癌症有关，包括结直肠癌（CRC）。在这里，我们调查了异常的miR-142-3p表达及其在主要CRC样本中的可能功能后果。方法采用定量RT-PCR技术检测116例原发性CRC组织及附近非肿瘤组织中miR-142-3p的表达。通过细胞活力和集落形成测定，通过异种移植裸鼠体内生长，体外评估miR-142-3p在CRC衍生细胞中上调或下调的作用。结果使用定量RT-PCR，我们发现与相邻的非肿瘤组织相比，miR-142-3p在78.4％（91/116）的主要CRC组织中被下调。我们还发现，miR-142-3p模拟物通过在CRC衍生的细胞中诱导细胞周期停滞来降低体外细胞活力和集落形成，并抑制异种移植裸鼠体内肿瘤细胞的生长。相反，我们发现miR-142-3p抑制剂增加了异种移植裸鼠中CRC衍生细胞的活力和集落形成能力以及肿瘤细胞的生长。此外，我们通过预测和双荧光素酶报告基因分析将CDK4鉴定为miR-142-3p的潜在靶标。一致地，我们发现miR-142-3p模拟物和抑制剂可以分别降低和增加CRC衍生细胞中CDK4蛋白的水平。结论根据我们的研究结果，我们得出结论，miR-142-3p可能在CRC中起着抑癌作用，并且可以作为基于miRNA的CRC治疗的工具。

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