Yu Yue, Zhao Ying, Sun Xiao-Hu, Ge Jie, Zhang Bin, Wang Xin, Cao Xu-Chen
The First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin 300060, China.
Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China.
Oncotarget. 2015 Oct 27;6(33):34423-36. doi: 10.18632/oncotarget.5406.
The epithelial to mesenchymal transition (EMT) plays a pivotal role in breast cancer progression. We found that overexpression of miR-129-5p reversed EMT, whereas depletion of miR-129-5p induced EMT in breast cancer cells. We demonstrated that Twist1 is a direct target of miR-129-5p. Both Twist1 and Snail transcriptionally suppressed miR-129-5p expression. Levels of miR-129-5p were low in breast cancer tissues. miR-129-5p down-regulation correlated with advanced clinical stage and poor prognosis in patients with breast cancer. miR-129-5p expression negatively correlated with Twist1 and Snail expression. Thus, miR-129-5p down-regulation fosters EMT in breast cancer by increasing Twist1-Snail and activating a negative feedback loop.
上皮-间质转化(EMT)在乳腺癌进展中起关键作用。我们发现,miR-129-5p的过表达逆转了EMT,而miR-129-5p的缺失则在乳腺癌细胞中诱导了EMT。我们证明Twist1是miR-129-5p的直接靶点。Twist1和Snail均转录抑制miR-129-5p的表达。miR-129-5p在乳腺癌组织中的水平较低。miR-129-5p的下调与乳腺癌患者的晚期临床分期和不良预后相关。miR-129-5p的表达与Twist1和Snail的表达呈负相关。因此,miR-129-5p的下调通过增加Twist1-Snail并激活负反馈环促进乳腺癌中的EMT。