Ji Chunmei, Liu Hang, Yin Qiang, Li Hui, Gao Han
Department of Clinical Laboratory, People's Hospital of Weifang, Weifang, Shandong, People's Republic of China.
Department of Interventional Therapy, Yidu Central Hospital of Weifang, Weifang, Shandong, People's Republic of China.
Biotechnol Lett. 2017 Nov;39(11):1621-1629. doi: 10.1007/s10529-017-2403-5. Epub 2017 Jul 26.
To clarify the potential biological function of miR-93 and its related molecular mechanism underlying metastasis in human hepatocellular carcinoma (HCC).
miR-93 was significantly up-regulated in HCC tissues and was associated with poor 5-year overall survival in HCC patients. Transwell assays showed that over-expression of miR-93 increased HCC cell migration and invasion in vitro. Programmed cell death 4 (PDCD4) was a target gene of miR-93 and miR-93 could down-regulate the expression of PDCD4 by directly targeting its 3'-UTR. The re-expression of PDCD4 could attenuate the HCC cell invasion and migration induced by miR-93, while the knockdown of PDCD4 would promote HCC cell migration and invasion via the epithelial-mesenchymal transition (EMT) pathway.
miR-93 provides new insight into the molecular mechanisms of pathogenesis and progression in HCC and offer a potential therapeutic target for the treatment of HCC patients.
阐明miR-93在人肝细胞癌（HCC）转移中的潜在生物学功能及其相关分子机制。
miR-93在HCC组织中显著上调，且与HCC患者5年总生存率低相关。Transwell实验表明，miR-93过表达增加了HCC细胞的体外迁移和侵袭能力。程序性细胞死亡4（PDCD4）是miR-93的靶基因，miR-93可通过直接靶向其3'-UTR下调PDCD4的表达。PDCD4的重新表达可减弱miR-93诱导的HCC细胞侵袭和迁移，而敲低PDCD4则会通过上皮-间质转化（EMT）途径促进HCC细胞迁移和侵袭。
miR-93为HCC发病机制和进展的分子机制提供了新的见解，并为HCC患者的治疗提供了潜在的治疗靶点。
