MicroRNA‐106b targets FUT6 to promote cell migration, invasion, and proliferation in human breast cancer. Issue 9 (13th August 2016)

• Record Type: Journal Article
• Authors: Li, Nana; Liu, Yuejian; Miao, Yuan; Zhao, Lifen; Zhou, Huimin; Jia, Li
• Is Part Of: IUBMB life. Volume 68:Issue 9(2016)
• Page Start: 764
• Page End: 775
• Publication Date: 2016-08-13
• Subjects: microRNA‐106b -- breast cancer -- FUT6 -- migration -- invasion -- proliferation; Biochemistry -- Periodicals; Molecular biology -- Periodicals; 572.8
• DOI: 10.1002/iub.1541
• Languages: English
• ISSNs: 1521-6543

Abstract

Abstract: It is demonstrated that the maladjustment of microRNA (miRNA) plays significant roles in the occurrence and development of tumors. MicroRNA‐106b‐5p (miR‐106b), a carcinogenic miRNA, is identified as a dysregulated miRNA in human breast cancer. In this article, the expression levels of miR‐106b were discovered to be particularly higher in breast cancer tissues than that in the corresponding adjacent tissues. Accordingly, miR‐106b was higher expressed in the breast cancer cell lines compared with that in the normal breast cell lines. Moreover, according to the data previously reported, increased expression of miR‐106b was significantly associated with advanced clinical stages and poor prognosis in breast cancer. Fucosyltransferase 6 (FUT6), a member of the fucosyltransferase (FUT) family, was found to have a reduced expression in tissues or cells with higher level of miR‐106b in breast cancer. Additionally, down‐regulation of miR‐106b increased the expression of FUT6 and resulted in an obvious decrease of cell migration, invasion, and proliferation in MDA‐MB‐231 cells. Furthermore, over‐expressed FUT6 reversed the impacts of up‐regulated miR‐106b on cell migration, invasion, and proliferation in MCF‐7 cells, indicating that FUT6 might be directly targeted by miR‐106b and serve as therapeutic targets for breast cancer. In brief, our results strongly showed that the low expression of FUT6 regulated by miR‐106b contributed to cell migration, invasion, and proliferation in human breast cancer. © 2016 IUBMB Life, 68(9):764–775, 2016