CircUBXN7 suppresses cell proliferation and facilitates cell apoptosis in lipopolysaccharide-induced cell injury by sponging miR-622 and regulating the IL6ST/JAK1/STAT3 axis
CircUBXN7 suppresses cell proliferation and facilitates cell apoptosis in lipopolysaccharide-induced cell injury by sponging miR-622 and regulating the IL6ST/JAK1/STAT3 axis
复制标题
CircUBXN7 通过海绵 miR-622 和调节 IL6ST/JAK1/STAT3 轴来抑制脂多糖诱导的细胞损伤中的细胞增殖并促进细胞凋亡。
DOI：
10.1016/j.biocel.2022.106313
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发表时间：
2022-10-19
影响因子：
4
通讯作者：
Zhu, Lei
中科院分区：
文献类型：
--
作者：
Xu, Fan;Chen, Runnan;Zhu, Lei
急性呼吸窘迫综合征（Acute respiratory distress syndrome， ARDS）是一种常见的严重呼吸系统疾病，发病率和死亡率都很高。环状rna已被证明参与各种疾病过程。然而，大多数环状rna在ARDS中的生物学功能和机制尚未阐明。在本研究中，我们发现cirbxn7在脂多糖（LPS）诱导的A549和Beas-2B细胞损伤中显著升高。在lps诱导的A549和Beas-2B细胞中，抑制circUBXN7可显著促进细胞增殖，减少细胞凋亡，而过表达circUBXN7可抑制细胞增殖，加速细胞凋亡。CircUBXN7作为miR-622的海绵，miR-622挽救了CircUBXN7对细胞增殖和凋亡的影响。我们还发现IL6ST是miR-622的靶基因，并且IL6ST的表达受到cirbxn7的间接调控。此外，western blotting显示，在lps诱导的A549和Beas-2B细胞损伤中，JAK1/STAT3信号通路参与了circUBXN7/miR-622/IL6ST轴。综上所述，我们的研究表明，在lps诱导的A549和Beas-2B细胞损伤中，circUBXN7通过海绵化miR-622和调节IL6ST来抑制细胞增殖，促进细胞凋亡，激活JAK1/STAT3信号通路。因此，cirbxn7可能是ARDS的潜在生物标志物，cirbxn7的失调可能参与了ARDS的发病机制。
Acute respiratory distress syndrome (ARDS) is a common and serious respiratory illness with substantial morbidity and mortality. Circular RNAs have been demonstrated to participate in various diseases processes. However, the biological function and mechanism of most circular RNAs have not been elucidated in ARDS. In this study, we found that circUBXN7 was significantly increased in lipopolysaccharide (LPS)-induced A549 and Beas-2B cell injury. Inhibition of circUBXN7 significantly promoted cell proliferation and reduced cell apoptosis, while overexpression of circUBXN7 suppressed cell proliferation and accelerated cell apoptosis in LPS-induced A549 and Beas-2B cells. CircUBXN7 acted as a sponge for miR-622, and miR-622 rescued the effect of circUBXN7 on cell proliferation and apoptosis. We also found that IL6ST was a target gene of miR-622, and the expression of IL6ST was indirectly regulated by circUBXN7. Furthermore, western blotting indicated that the JAK1/STAT3 signaling pathway was involved in the circUBXN7/miR-622/IL6ST axis in LPS-induced A549 and Beas-2B cell injury. Overall, our study suggested that circUBXN7 suppressed cell proliferation and facilitated cell apoptosis by sponging miR-622 and regulating IL6ST, to activate the JAK1/STAT3 signaling pathway in LPS-induced A549 and Beas-2B cell injury. CircUBXN7 might therefore be a potential biomarker for ARDS, and dysregulation of circUBXN7 may be involved in the pathogenesis of ARDS.