School of Life Sciences, Jiangsu Normal University, Xuzhou 221116, China.
School of Life Sciences, Shandong University of Technology, Zibo 225000, China.
Biosci Rep. 2021 Aug 27;41(8). doi: 10.1042/BSR20210318.
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.
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。
