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Cited by 45MicroRNA in disease regulationCancer-related Molecular PathwaysCell death mechanisms and regulation

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

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Li, Jincheng, Aung, Lynn Htet Htet, Long, Bo, Qin, Danian, An, Shejuan, Li, Peifeng·2015·Scientific Reports
DOI 10.1038/srep16422PMC PMC4639766
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Abstract

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.

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  • Overexpression of miR-23a-3p can promote cell viability and repress apoptosis.

    “Additionally, there are certain studies explicit that overexpression of miR-23a-3p can promote cell viability as well as repressed apoptosis.”

    From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [61]

    The Results section, “miR-23a participates in the regulation of apoptosis” (page not supplied), reports the opposite of the claimed effect: miR-23a overexpression sensitized cardiomyocytes to apoptosis induced by hydrogen peroxide or doxorubicin. The supplied passages do not report increased cell viability or establish that the tested miR-23a was specifically miR-23a-3p. (LLM, conf=0.90)

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  • In rats with myocardial ischemia-reperfusion injury, miR-23 can target FoxO3a to regulate cardiomyocyte growth, leading to increased cardiomyocyte apoptosis, while overexpression of miR-23 effectively reduced this phenomenon.

    “In rats with myocardial ischemia-reperfusion injury, it can target FoxO3a to regulate cardiomyocyte growth, leading to increased cardiomyocyte apoptosis while the overexpression of miR-23 effectively reduced this phenomenon [[60], [61], [62]].”

    From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [61]

    The Results (page not provided) report the opposite effect: miR-23a overexpression increased cardiomyocyte susceptibility to apoptosis after hydrogen peroxide or doxorubicin treatment, while knockdown reduced apoptosis. The Methods describe cultured neonatal rat cardiomyocytes, not rats with myocardial ischemia-reperfusion injury; the Discussion identifies a p53/miR-128 pathway rather than FoxO3a. (LLM, conf=0.90)

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  • miR-23a specifically binds to p53 to stimulate its transcriptional activity in cardiomyocytes and promotes oxidative stress-induced cell apoptosis.

    “it also specifically binds to p53 to stimulate its transcriptional activity in cardiomyocytes and promotes oxidative stress-induced cell apoptosis.”

    From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [61]

  • miR-23a inhibits cigarette smoke extract-induced pulmonary vascular endothelial cell apoptosis by targeting DNAJB1, thus alleviating pulmonary emphysema development.

    “For instance, miR-23a inhibits cigarette smoke extract-induced pulmonary vascular endothelial cell apoptosis by targeting DNAJB1, thus alleviating pulmonary emphysema development;”

    From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [61]

    The Results section reports that miR-23a promotes hydrogen peroxide- or doxorubicin-induced apoptosis in cardiomyocytes. Our copy does not address cigarette smoke extract, pulmonary vascular endothelial cells, DNAJB1, or emphysema; the finding in a different cell type and condition does not establish or contradict the attributed claim. (LLM, conf=0.75)

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Authors
Li, J., Aung, L. H. H., Long, B., Qin, D., An, S., & Li, P.
Affiliations
  • Shantou University (CN)
  • University of Illinois Chicago (US)
  • Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
Corresponding author
  • Qin, Danian
  • Li, Peifeng
ORCID
Venue
Scientific Reports
Publisher
Springer Science and Business Media LLC
Published
2015-11-10
Volume
5
Issue
1
Pages
16422-16422
ISSN
2045-2322 (ISSN-L)
DOI
10.1038/srep16422
PMC
PMC4639766
OpenAlex
W2134536196
Cited by
45
References
51
Citations by year
2025: 2 · 2024: 9 · 2023: 2 · 2022: 5 · 2021: 6 · 2020: 4 · 2019: 4 · 2018: 3 · 2017: 8 · 2016: 2
FWCI
1.43
Type
journal article
Language
en
Open access
Licence
Locations
  • Scientific Reports (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Figshare (submittedVersion, cc-by)
Funders
  • National Institutes of Health
  • National Key Research and Development Program of China (2007CB512000)
  • National Heart, Lung, and Blood Institute (R01HL102202)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
miR-23a, p53, miR-128, prohibitin, apoptosis, cardiomyocytes, oxidative stress, transcriptional regulation, miRNA-mRNA interactions, cardiac pathology
MeSH terms
Prohibitins, Animals, Base Sequence, Binding Sites, Gene Expression Regulation, Promoter Regions, Genetic, Protein Binding, Repressor Proteins, RNA, Messenger, Transcriptional Activation, Tumor Suppressor Protein p53, Apoptosis, RNA Interference, MicroRNAs, Rats

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