miR-23a binds to p53 and enhances its association with miR-128 promoter.
miR-23a binds to p53 and enhances its association with miR-128 promoter.
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DOI：
10.1038/srep16422
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发表时间：
2015-11-10
影响因子：
4.6
通讯作者：
Li P
中科院分区：
文献类型：
--
作者：
Li J;Aung LH;Long B;Qin D;An S;Li P
细胞凋亡在心脏病理学中发挥着重要作用，但细胞凋亡调节的分子机制在很大程度上仍不清楚。在这里，我们报道 miR-23a 促进 p53 在心肌细胞中的凋亡作用。我们的结果表明，miR-23a 促进氧化应激诱导的细胞凋亡。在探索 miR-23a 促进细胞凋亡的分子机制时，我们发现它使 p53 对 miR-128 调节的作用敏感。它促进p53与miR-128启动子区域的结合，并增强p53对miR-128表达的转录激活。 miR-128可以下调抑制素的表达，从而促进细胞凋亡。我们的数据提供了新的证据，表明 miR-23a 可以刺激 p53 的转录活性。
Apoptosis plays an important role in cardiac pathology, but the molecular mechanism by which apoptosis regulated remains largely elusive. Here, we report that miR-23a promotes the apoptotic effect of p53 in cardiomyocytes. Our results showed that miR-23a promotes apoptosis induced by oxidative stress. In exploring the molecular mechanism by which miR-23a promotes apoptosis, we found that it sensitized the effect of p53 on miR-128 regulation. It promoted the association of p53 to the promoter region of miR-128, and enhanced the transcriptional activation of p53 on miR-128 expression. miR-128 can downregulate prohibitin expression, and subsequently promote apoptosis. Our data provides novel evidence revealing that miR-23a can stimulate transcriptional activity of p53.