Ming Zhang, Baochang Shi, Kai Zhang

Oncology Research, Vol.27, No.9, pp. 1061-1068, 2019, DOI:10.3727/096504019X15565325878380

Abstract Deregulation of miR-186 and Twist1 has been identified to be involved in the progression of multiple cancers. However, the detailed molecular mechanisms underlying miR-186-involved cholangiocarcinoma (CCA) are still unknown. In this study, we found that miR-186 was downregulated in CCA tissues and cell lines, and negatively correlated with the expression of Twist1 protein. In vitro assays demonstrated that miR-186 mimics repressed cell proliferation, in vivo tumor formation, and caused cell cycle arrest. miR-186 mimics also inhibited the migration and invasion of CCLP1 and SG-231 cells. Mechanistically, the 3′-untranslated region (3′-UTR) of Twist1 mRNA is a direct target of miR-186. Further,… More >

Junfeng Lu^*, Zhongsong Zhao^†, Yanhong Ma^‡

Oncology Research, Vol.28, No.5, pp. 509-518, 2020, DOI:10.3727/096504020X15954139263808

Abstract The present study aimed to investigate the effect of miR-186 on proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) of hepatocellular carcinoma (HCC). In this work, miR-186 was downregulated in HCC tissues and cells, and low miR-186 level helped predict the occurrence of vascular invasion and poor prognosis in patients with HCC. miR-186 overexpression inhibited cell proliferation and tumor growth in nude mice, repressed migration and invasion abilities, and enhanced apoptosis in HCC cells. miR-186 also retarded progression of EMT. miR-186 directly bound to the 3 -untranslated regions of cyclin-dependent kinase 6 (CDK6) to inhibit its expression. Overexpression of CDK6 markedly… More >