MicroRNA-106b targets FUT6 to promote cell migration, invasion, and proliferation in human breast cancer

MicroRNA-106b targets FUT6 to promote cell migration, invasion, and proliferation in human breast cancer
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DOI:
10.1002/iub.1541
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发表时间:
2016-09-01
期刊:
影响因子:
4.6
通讯作者:
Jia, Li
Jia, Li
中科院分区:
生物学3区
文献类型:
--
作者:
Li, Nana;Liu, Yuejian;Jia, Li

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研究表明,microRNA (miRNA)的失调在肿瘤的发生发展中起着重要的作用。MicroRNA-106b-5p (miR-106b)是一种致癌miRNA,在人乳腺癌中被发现是一种失调的miRNA。在本文中,我们发现miR-106b在乳腺癌组织中的表达水平特别高于相应的癌旁组织。因此,miR-106b在乳腺癌细胞系中的表达高于正常乳腺细胞系。此外,根据先前报道的数据,miR-106b的表达升高与乳腺癌的晚期临床分期和不良预后显著相关。focusyltransferase 6 (FUT6)是focusyltransferase (FUT)家族的一员,在乳腺癌中miR-106b水平较高的组织或细胞中表达减少。此外,miR-106b的下调增加了FUT6的表达,导致MDA-MB-231细胞的细胞迁移、侵袭和增殖明显减少。此外,过表达的FUT6逆转了上调的miR-106b对MCF-7细胞迁移、侵袭和增殖的影响,这表明FUT6可能是miR-106b的直接靶点,可以作为乳腺癌的治疗靶点。总之,我们的研究结果强烈表明,miR-106b调控FUT6的低表达有助于人类乳腺癌细胞的迁移、侵袭和增殖。(c)生物工程学报,2016,36 (9):764-775,2016
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. (c) 2016 IUBMB Life, 68(9):764-775, 2016