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Research article
Aiqun Ma
First Affiliated Hospital of Xi'an Jiaotong University
Corresponding Author
ORCiD: https://orcid.org/0000-0003-3195-5013
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Non-coding RNA plays a critical role in myocardial apoptosis induced by doxorubicin (DOX). However, the specific function of Long noncoding RNA (lncRNA) small ubiquitin-like modifier 1 pseudogene 3 (SUMO1P3) is unclear. The purpose of this study was to determine the role of lncRNA SUMO1P3 in myocardial apoptosis induced by DOX.
Methods: QRT-PCR were used to detect the expression levels of SUMO1P3 and miR-93-5p in DOX-treated primary cardiomyocytes and rat models. QRT-PCR and Western blot were used to detect the expression levels of Bin1 in DOX-treated primary cardiomyocytes and rat models. The relationship between SUMO1P3, miR-93-5p and Bin1 was analyzed using bioinformatics analysis and Luciferase reporter assay. The effects of DOX on the viability and apoptosis of cardiomyocytes were evaluated by flow cytometry and CCK-8. The effects of SUMO1P3 on cardiomyocyte apoptosis were analyzed by TUNEL staining and echocardiography.
Results: In DOX-treated primary cardiomyocytes and rat models, the expression levels of SUMO1P3 and Bin1 were significantly increased, while the expression levels of miR-93-5p were significantly reduced. MiR-93-5p was a direct target gene of SUMO1P3, and Bin1 was a direct target gene of miR-93-5p. In addition, miR-93-5p reversed the protective effect of SUMO1P3 knockout on cardiomyocytes by inhibiting the expression of Bin1.
Conclusions: SUMO1P3 inhibited DOX-induced cardiomyocyte apoptosis through miR-93-5p/Bin1 axis.
Keywords
SUMO1P3, miR-93-5p, Bin1, DOX, cardiomyocytes
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This is a preprint. It has not completed peer review.
Research article
Aiqun Ma
First Affiliated Hospital of Xi'an Jiaotong University
Corresponding Author
ORCiD: https://orcid.org/0000-0003-3195-5013
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 2
Posted 10 Mar, 2021
No community comments so far
No comments provided
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Molecular Biology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Non-coding RNA plays a critical role in myocardial apoptosis induced by doxorubicin (DOX). However, the specific function of Long noncoding RNA (lncRNA) small ubiquitin-like modifier 1 pseudogene 3 (SUMO1P3) is unclear. The purpose of this study was to determine the role of lncRNA SUMO1P3 in myocardial apoptosis induced by DOX.
Methods: QRT-PCR were used to detect the expression levels of SUMO1P3 and miR-93-5p in DOX-treated primary cardiomyocytes and rat models. QRT-PCR and Western blot were used to detect the expression levels of Bin1 in DOX-treated primary cardiomyocytes and rat models. The relationship between SUMO1P3, miR-93-5p and Bin1 was analyzed using bioinformatics analysis and Luciferase reporter assay. The effects of DOX on the viability and apoptosis of cardiomyocytes were evaluated by flow cytometry and CCK-8. The effects of SUMO1P3 on cardiomyocyte apoptosis were analyzed by TUNEL staining and echocardiography.
Results: In DOX-treated primary cardiomyocytes and rat models, the expression levels of SUMO1P3 and Bin1 were significantly increased, while the expression levels of miR-93-5p were significantly reduced. MiR-93-5p was a direct target gene of SUMO1P3, and Bin1 was a direct target gene of miR-93-5p. In addition, miR-93-5p reversed the protective effect of SUMO1P3 knockout on cardiomyocytes by inhibiting the expression of Bin1.
Conclusions: SUMO1P3 inhibited DOX-induced cardiomyocyte apoptosis through miR-93-5p/Bin1 axis.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
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