Long Noncoding RNA SOX2-OT Aggravates Doxorubicin-Induced Apoptosis of Cardiomyocyte by Targeting miR-942-5p/DP5

被引:19
作者
Wang, Haining [1 ]
Lin, Xiule [1 ]
Li, Jilin [2 ]
Zeng, Guoning [1 ]
Xu, Tan [1 ]
机构
[1] Shantou Univ, Affiliated Hosp 1, Med Coll, Cardiac Care Unit CCU,Dept Cardiovasc Med, Shantou 515041, Guangdong, Peoples R China
[2] Shantou Univ, Affiliated Hosp 2, Med Coll, Dept Cardiovasc Med, Shantou 515000, Guangdong, Peoples R China
关键词
lncRNA SOX2-OT; miR-942-5p; DP5; cardiomyocyte; apoptosis; BREAST-CANCER; HEART-FAILURE; MIRNAS; IDENTIFICATION; ACTIVATION; EXPRESSION; BIOMARKERS; GENE; JNK;
D O I
10.2147/DDDT.S267474
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Background: Long non-coding RNAs (LncRNAs) play important roles in doxorubicin (DOX)-induced apoptosis of cardiomyocytes. However, the function of lncRNA SOX2-OT is unclear. This study was carried out to investigate the function of SOX2-OT in doxorubicin-induced cardiomyocyte apoptosis. Methods: qRT-PCR and immunoblotting were used to detect the expression levels of SOX2-OT, miR-942-5p and death protein-5 (DP5) in DOX-treated primary cardiomyocytes and rat models. The relationship among miR-942-5p, SOX2-OT, and DP5 was explored by luciferase reporter assay. The effects of SOX2-OT, miR-942-5p and DP5 on doxorubicin-induced cardiomyocyte apoptosis were evaluated by Annexin V-FITC/PI method and caspase-3 activity assay. The effect of SOX2-OT on cardiomyocyte apoptosis was analyzed by TUNEL staining and echocardiography. Results: SOX2-OT and DP5 were highly expressed, while miR-942-5p was down-regulated in DOX-treated primary cardiomyocytes and rat model. SOX2-OT can upregulate DP5 as a sponge of miR-942-5p, which was a direct target of miR-942-5p. In addition, miR-942-5p reversed the protective effect of knockdown of SOX2-OT on cardiomyocytes by inhibiting the expression of DP5 in vitro and in vivo. Conclusion: Knockdown of SOX2-OT down-regulated DP5 via sponging miR-942-5p and inhibiting DOX-induced apoptosis of primary cardiomyocytes.
引用
收藏
页码:481 / 492
页数:12
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