This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
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, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
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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