• Xiangyu Zhu, Si-Ping Ma, Dongxiang Yang, Yanlong Liu, Yong-Peng Wang, Tao Lin, Yan-Xi Li, Shi-Hua Yang, Wan-Chuan Zhang, and Xin-Ling Wang.
• Department of Colorectal Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Insititute, Liaoning, China.
• Cell. Physiol. Biochem. 2018 Jan 1; 51 (4): 1969-1981.

Background/AimsDeregulation 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.MethodsThe 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.ResultsUsing 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.ConclusionFrom 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.© 2018 The Author(s). Published by S. Karger AG, Basel.

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