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miR-23a binds to p53 and enhances its association with miR-128 promoter.

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journal contribution
posted on 04.05.2016, 00:00 by J Li, LH Aung, B Long, D Qin, S An, P Li
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.


This work was supported by National Basic Research Program of China (973 Program, 2007CB512000), a grant 5R01HL102202 from the National Institutes of Health, Bethesda, MD, and a grant from American Cancer Society (120861).


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This is a copy of an article published in Scientific Reports © 2015 Nature Publishing Group Publications.


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