Key Laboratory of Resource Biology and Biotechnology, School of Life Sciences, Northwest University, Xi'an, China.
Institute of Preventive Genomic Medicine, Northwest University, Xi'an, China.
J Biochem Mol Toxicol. 2019 Jun;33(6):e22308. doi: 10.1002/jbt.22308. Epub 2019 Feb 15.
Mutations in transforming growth factor beta receptor II (TGFBR2) are detected in up to 30% of overall colorectal cancer (CRC). Dysregulation of some microRNAs participated in the CRC pathogenesis. In this study, we used the gene ontology analyses, the Kyoto Encyclopedia of Genes and Genomes pathway analyses and gene set enrichment analysis to indicate that miR-3191 was involved in the regulation of transforming growth factor beta (TGF-BETA) signal pathway in CRC. These bioinformatics results were supported by data obtained from CRC samples and experiments in vitro. The luciferase reporter assay was used to confirm that miR-3191 modulates TGF-BETA signal pathway by targeting TGFBR2. By transwell migration and invasion assays, we showed that miR-3191 promoted CRC cell migration and invasion by downregulating TGFBR2. And it may serve as a novel therapeutic strategy for treating CRC patients.
转化生长因子-β受体 II (TGFBR2) 突变在高达 30%的结直肠癌 (CRC) 中被检测到。一些 microRNAs 的失调参与了结直肠癌的发病机制。在这项研究中，我们使用基因本体分析、京都基因与基因组百科全书通路分析和基因集富集分析表明，miR-3191 参与了结直肠癌中转化生长因子-β (TGF-BETA) 信号通路的调节。这些生物信息学结果得到了结直肠癌样本和体外实验数据的支持。荧光素酶报告基因检测证实 miR-3191 通过靶向 TGFBR2 来调节 TGF-BETA 信号通路。通过 Transwell 迁移和侵袭实验，我们表明 miR-3191 通过下调 TGFBR2 促进 CRC 细胞的迁移和侵袭。它可能成为治疗 CRC 患者的一种新的治疗策略。
