MicroRNA-96-5p represses breast cancer proliferation and invasion through Wnt/β-catenin signaling via targeting CTNND1
MicroRNA-96-5p represses breast cancer proliferation and invasion through Wnt/β-catenin signaling via targeting CTNND1
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DOI：
10.1038/s41598-019-56571-z
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发表时间：
2020-01-08
影响因子：
4.6
通讯作者：
Guo, Yan-zhen
中科院分区：
文献类型：
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作者：
Gao, Xiao-hui;Zhang, Ya-li;Guo, Yan-zhen
MiR-96-5p低表达是许多癌症的特征，但它在乳腺癌(BCA)中的作用尚不清楚。在这里，我们评估了miR-96-5p在BC发育中的作用。我们证明外源表达miR-96-5p可以抑制BCA细胞的增殖、迁移和侵袭能力。在机制上，BCA细胞中的miR-96-5p靶向并下调连环蛋白增量1(CTNND1)，导致β-连环蛋白表达降低，WNT11信号丢失，细胞周期蛋白D1水平降低，MMP7表达降低。外源表达CTNND1可以减轻这些影响。综上所述，我们首次发现miR-96-5p通过靶向CTNND1和随后的Wnt/β-catenin信号通路抑制BCA细胞的增殖、侵袭和迁移表型。这些数据突出了miR-96-5P作为BC治疗的新靶点。
Low miR-96-5p expression is characteristic of many cancers but its role in breast cancer (BCa) remains poorly defined. Here, the role of miR-96-5p in BC development was assessed. We demonstrate that exogenously expressing miR-96-5p inhibits the proliferative, migratory and invasive capacity of BCa cells. Mechanistically, miR-96-5p in BCa cells was found to target and downregulate catenin delta 1 (CTNND1) leading to decreased beta-catenin expression, a loss of WNT11 signaling, reduced cyclin D1 levels and lower MMP7 expression. Exogenously expressing CTNND1 alleviated these effects. In summary, we are the first to reveal that miR-96-5p inhibits the proliferative, invasive and migratory phenotypes of BCa cells the targeting of CTNND1 and subsequent Wnt/beta-catenin signaling. These data highlight miR-96-5p as a novel target for BC treatment.