LncRNA SUMO1P3 aggravates doxorubicin-induced cardiomyocyte apoptosis by targeting miR-93-5p / Bin1

Abstract 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.