OBJECTIVES To investigate the effect of long non-coding (lnc) RNA PVT1 on apoptosis induced by doxorubicin-induced cardiotoxicity. METHODS We analyzed the expression levels of lncRNA PVT1, miR-187-3p, using reverse transcription real-time quantitative PCR (RT-qPCR) in doxorubicin-treated cardiomyocytes. The mechanism of lncRNA PVT1 in cardiotoxicity was investigated using cell transfection, CCK-8, flow cytometry, Western blot, and dual-luciferase reporter assays. RESULTS Doxorubicin promotes H9c2 apoptosis and increased PVT1 expression in cardiomyocytes. Knockdown of PVT1 attenuated doxorubicin-induced cardiomyocyte apoptosis. We found that miR-187-3p is a direct target of PVT1, and that lncRNA PVT1 adsorbs miR-187-3p by sponge action, reducing miR-187-3p levels. miR-187-3p negatively regulates AGO1, and PVT1 regulates AGO1 expression by targeting miR-187-3p, thereby regulating apoptosis. In addition, we knocked down AGO1 in H9c2 cells transfected with the miR-187-3p inhibitor, and found that it inhibited apoptosis. CONCLUSION In doxorubicin-induced cardiomyocyte toxicity, the highly expressed lncRNA PVT1 enhances the expression of AGO1 by sponge adsorption of miR-187-3p. Decreasing the expression of lncRNA PVT1 inhibits the adsorption of miR-187-3p through competing endogenous (ce) RNA, thereby reducing the expression of AGO1 and decreasing the apoptosis of cardiomyocytes.

中文翻译：

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lncRNA PVT1通过靶向miR-187-3p / AGO1轴来加剧阿霉素诱导的心肌细胞凋亡。

目的研究长非编码（lnc）RNA PVT1对阿霉素诱导的心脏毒性诱导的细胞凋亡的影响。方法我们使用逆转录实时定量PCR（RT-qPCR）分析了阿霉素处理过的心肌细胞中lncRNA PVT1，miR-187-3p的表达水平。使用细胞转染，CCK-8，流式细胞仪，Western印迹和双荧光素酶报告基因检测法研究了lncRNA PVT1的心脏毒性机制。结果阿霉素可促进心肌细胞中H9c2凋亡并增加PVT1表达。击倒PVT1减弱了阿霉素诱导的心肌细胞凋亡。我们发现miR-187-3p是PVT1的直接靶标，而lncRNA PVT1通过海绵作用吸附miR-187-3p，从而降低了miR-187-3p的水平。miR-187-3p负调节AGO1，PVT1通过靶向miR-187-3p来调节AGO1的表达，从而调节细胞凋亡。此外，我们敲低了用miR-187-3p抑制剂转染的H9c2细胞中的AGO1，发现它可以抑制细胞凋亡。结论在阿霉素诱导的心肌细胞毒性中，高表达的lncRNA PVT1通过海绵吸附miR-187-3p增强了AGO1的表达。降低lncRNA PVT1的表达可抑制miR-187-3p通过竞争性内源（ce）RNA的吸附，从而降低AGO1的表达并减少心肌细胞的凋亡。高表达的lncRNA PVT1通过海绵吸附miR-187-3p增强AGO1的表达。降低lncRNA PVT1的表达可抑制miR-187-3p通过竞争性内源（ce）RNA的吸附，从而降低AGO1的表达并减少心肌细胞的凋亡。高表达的lncRNA PVT1通过海绵吸附miR-187-3p增强AGO1的表达。降低lncRNA PVT1的表达可抑制miR-187-3p通过竞争性内源（ce）RNA的吸附，从而降低AGO1的表达并减少心肌细胞的凋亡。