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miR-219-5p 靶向 TBXT,抑制乳腺癌细胞 EMT 及细胞迁移和侵袭。

miR-219-5p targets TBXT and inhibits breast cancer cell EMT and cell migration and invasion.

机构信息

School of Life Sciences, Jiangsu Normal University, Xuzhou 221116, China.

School of Life Sciences, Shandong University of Technology, Zibo 225000, China.

出版信息

Biosci Rep. 2021 Aug 27;41(8). doi: 10.1042/BSR20210318.

Abstract

miR-219-5p has been reported to act as either a tumor suppressor or a tumor promoter in different cancers by targeting different genes. In the present study, we demonstrated that miR-219-5p negatively regulated the expression of TBXT, a known epithelial-mesenchymal transition (EMT) inducer, by directly binding to TBXT 3'-untranslated region. As a result of its inhibition on TBXT expression, miR-219-5p suppressed EMT and cell migration and invasion in breast cancer cells. The re-introduction of TBXT in miR-219-5p overexpressing cells decreased the inhibitory effects of miR-219 on EMT and cell migration and invasion. Moreover, miR-219-5p decreased breast cancer stem cell (CSC) marker genes expression and reduced the mammosphere forming capability of cells. Overall, our study highlighted that TBXT is a novel target of miR-219-5p. By suppressing TBXT, miR-219-5p plays an important role in EMT and cell migration and invasion of breast cancer cells.

摘要

miR-219-5p 通过靶向不同的基因,在不同的癌症中既可以作为肿瘤抑制因子,也可以作为肿瘤促进因子。在本研究中,我们证明 miR-219-5p 通过直接结合 TBXT 的 3'-非翻译区,负调控 TBXT 的表达,TBXT 是一种已知的上皮间质转化(EMT)诱导剂。由于对 TBXT 表达的抑制,miR-219-5p 抑制了乳腺癌细胞中的 EMT 和细胞迁移及侵袭。在 miR-219-5p 过表达的细胞中转染 TBXT 后,降低了 miR-219 对 EMT 和细胞迁移及侵袭的抑制作用。此外,miR-219-5p 降低了乳腺癌干细胞(CSC)标志物基因的表达,并降低了细胞的成球能力。总之,我们的研究强调了 TBXT 是 miR-219-5p 的一个新靶点。通过抑制 TBXT,miR-219-5p 在乳腺癌细胞的 EMT 和细胞迁移及侵袭中发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d4/8360836/3c89ea4c2835/bsr-41-bsr20210318-g1.jpg

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