Huang Lingli, Huang Lingwei, Li Ziwei, Wei Qing
Department of Pharmacy, Jiangsu Cancer Hospital and Jiangsu Institute of Cancer Research and the Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, Jiangsu 210009, P.R. China.
Department of Applied Physics, University of Eastern Finland, 70211 Kuopio, Finland.
Crit Rev Eukaryot Gene Expr. 2019;29(6):521-528. doi: 10.1615/CritRevEukaryotGeneExpr.2019030056.
MicroRNAs (miRNAs) are highly conserved short noncoding RNAs with the capacity of regulating gene expression posttranscriptionally. In this process, miRNAs partially bind complementary sites of target mRNAs. Among miRNAs, miR-493 performs important functions under diverse physiological conditions and participates in different pathogeneses, including pancreatic cancer, gastric cancer, and breast cancer. Differential expression of miR-493 plays a vital role in the generation, metastasis, and recurrence of tumors. Above all, increasing evidence indicates that miR-493 inhibits the generation and development of tumors by activating the Wnt/Β-catenin, Wnt/PCP, MEK/ERK, or PI3K/AKT signaling pathway, suggesting possibilities for miR-493 as an effective adjuvant cancer therapy. In this review, we discuss and summarize the biological mechanisms of miR-493 and its potential in cancer therapy. This review may provide a better understanding of the biological functions of miR-493 in tumors and provide important clues to cancer treatment.
微小RNA（miRNA）是高度保守的短链非编码RNA，具有在转录后调节基因表达的能力。在此过程中，miRNA与靶mRNA的互补位点部分结合。在miRNA中，miR-493在多种生理条件下起重要作用，并参与不同的发病机制，包括胰腺癌、胃癌和乳腺癌。miR-493的差异表达在肿瘤的发生、转移和复发中起着至关重要的作用。最重要的是，越来越多的证据表明，miR-493通过激活Wnt/β-连环蛋白、Wnt/平面细胞极性（PCP）、丝裂原活化蛋白激酶/细胞外信号调节激酶（MEK/ERK）或磷脂酰肌醇-3-激酶/蛋白激酶B（PI3K/AKT）信号通路来抑制肿瘤的发生和发展，这表明miR-493作为一种有效的辅助癌症治疗手段具有可能性。在本综述中，我们讨论并总结了miR-493的生物学机制及其在癌症治疗中的潜力。本综述可能有助于更好地理解miR-493在肿瘤中的生物学功能，并为癌症治疗提供重要线索。
