Abstract：
Thyroid carcinoma (THCA) is a common malignancy of the endocrine system. Further understanding of the molecular mechanism underlying THCA is crucial to develop effective diagnostic therapy and improve its treatments. In this study, we intended to provide novel direction for THCA targeted therapy from the aspect of lncRNA-miRNA-mRNA interaction. We aimed to investigate the function and molecular mechanism of lncRNA ATP1A1-AS1 in THCA.
Gene expression was assessed by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Cell growth was detected by CCK-8 and EdU assays. Flow cytometry was applied for analyzing cell apoptosis. The binding of ATP1A1-AS1 or IRF2BP2 to miR-620 was validated by RNA pulldown and luciferase reporter assays. The protein levels were examined by western blotting.
ATP1A1-AS1 was decreased in THCA cells and tissues. ATP1A1-AS1 overexpression attenuated cell growth and promoted apoptosis. MiR-620, which was upregulated in THCA, was identified as a direct target of ATP1A1-AS1. Furthermore, IRF2BP2 was discovered to be a target of miR-620, which displayed low expression in THCA cells and tissues. Importantly, IRF2BP2 knockdown reversed the influence of ATP1A1-AS1 overexpression on THCA cell proliferation and apoptosis.
LncRNA ATP1A1-AS1 inhibited cell growth and promotes apoptosis in THCA via the miR-620/IRF2BP2 axis.
Gene expression was assessed by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Cell growth was detected by CCK-8 and EdU assays. Flow cytometry was applied for analyzing cell apoptosis. The binding of ATP1A1-AS1 or IRF2BP2 to miR-620 was validated by RNA pulldown and luciferase reporter assays. The protein levels were examined by western blotting.
ATP1A1-AS1 was decreased in THCA cells and tissues. ATP1A1-AS1 overexpression attenuated cell growth and promoted apoptosis. MiR-620, which was upregulated in THCA, was identified as a direct target of ATP1A1-AS1. Furthermore, IRF2BP2 was discovered to be a target of miR-620, which displayed low expression in THCA cells and tissues. Importantly, IRF2BP2 knockdown reversed the influence of ATP1A1-AS1 overexpression on THCA cell proliferation and apoptosis.
LncRNA ATP1A1-AS1 inhibited cell growth and promotes apoptosis in THCA via the miR-620/IRF2BP2 axis.
摘要：
背景：甲状腺癌（THCA）是内分泌系统的常见恶性肿瘤。进一步了解THCA的分子机制对于开发有效的诊断疗法和改进其治疗至关重要。在这项研究中,我们旨在从lncRNA-miRNA-mRNA相互作用的角度为THCA靶向治疗提供新的方向。我们旨在研究lncRNAATP1A1-AS1在THCA中的功能和分子机制。
方法:通过逆转录定量聚合酶链反应(RT-qPCR)评估基因表达。通过CCK-8和EdU测定检测细胞生长。流式细胞术用于分析细胞凋亡。ATP1A1-AS1或IRF2BP2与miR-620的结合通过RNA下拉和荧光素酶报告基因测定来验证。通过蛋白质印迹法检查蛋白质水平。
结果：ATP1A1-AS1在THCA细胞和组织中降低。ATP1A1-AS1过表达减弱细胞生长并促进细胞凋亡。在THCA中上调的MiR-620，被确定为ATP1A1-AS1的直接靶标。此外，IRF2BP2被发现是miR-620的靶标,其在THCA细胞和组织中显示低表达。重要的是,IRF2BP2敲低可逆转ATP1A1-AS1过表达对THCA细胞增殖和凋亡的影响。
结论：LncRNAATP1A1-AS1通过miR-620/IRF2BP2轴抑制细胞生长并促进细胞凋亡。
方法:通过逆转录定量聚合酶链反应(RT-qPCR)评估基因表达。通过CCK-8和EdU测定检测细胞生长。流式细胞术用于分析细胞凋亡。ATP1A1-AS1或IRF2BP2与miR-620的结合通过RNA下拉和荧光素酶报告基因测定来验证。通过蛋白质印迹法检查蛋白质水平。
结果：ATP1A1-AS1在THCA细胞和组织中降低。ATP1A1-AS1过表达减弱细胞生长并促进细胞凋亡。在THCA中上调的MiR-620，被确定为ATP1A1-AS1的直接靶标。此外，IRF2BP2被发现是miR-620的靶标,其在THCA细胞和组织中显示低表达。重要的是,IRF2BP2敲低可逆转ATP1A1-AS1过表达对THCA细胞增殖和凋亡的影响。
结论：LncRNAATP1A1-AS1通过miR-620/IRF2BP2轴抑制细胞生长并促进细胞凋亡。
