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环状 RNA 0001361/miR-490-5p/IGF2 轴调控神经母细胞瘤细胞的活力和凋亡。

Circ_0001361/miR-490-5p/IGF2 Axis Regulates the Viability and Apoptosis of Neuroblastoma Cells.

机构信息

Department of General Surgery, Children's Hospital Affiliated to Soochow University, Suzhou, China.

Department of General Surgery, Anhui Provincial Children's Hospital, Hefei, China.

出版信息

Neurochem Res. 2024 Nov;49(11):3060-3068. doi: 10.1007/s11064-024-04225-6. Epub 2024 Aug 7.

Abstract

BACKGROUND

Circular RNAs (circRNAs) are involved in the neuroblastoma (NB) development. Objectie: The study aimed to determine the biological behaviors of circ_0001361 and explore its underlying mechanism in NB.

METHODS

The circ_0001361, miR-490-5p, and IGF2 levels were measured using quantitative real-time polymerase chain reaction. Cellular processes were analyzed using MTT assay or fluorescence-activated cell sorting (FACS). Phosphorylated (p)-PI3K, p-AKT, Bax, and caspase-3 were tested by western blot. Dual-luciferase reporter analysis together with RNA pull-down analysis were utilized to evaluate the correlation of miR-490-5p and circ_0001361 or IGF2.

RESULTS

The results in this study illustrated that an elevation of circ_0001361 levels was observed in NB. Depletion of circ_0001361 suppressed the viability but facilitated apoptosis of NB cells. Circ_0001361 sponged miR-490-5p, which targeted to regulate IGF2. Inhibition of miR-490-5p rescued the effect induced by circ_0001361 knockdown, while deletion of IGF2 rescued the effect induced by the miR-490-5p inhibitor.

CONCLUSIONS

In summary, a loss of circ_0001361 inhibited NB progression via targeting the miR-490-5p/IGF2 axis, suggesting that circ_0001361 may be a novel therapeutical target of NB.

摘要

背景

环状 RNA(circRNAs)参与神经母细胞瘤(NB)的发展。目的:本研究旨在确定 circ_0001361 的生物学行为,并探讨其在 NB 中的潜在机制。

方法

采用实时定量聚合酶链反应检测 circ_0001361、miR-490-5p 和 IGF2 的水平。采用 MTT 检测或荧光激活细胞分选(FACS)分析细胞过程。采用 Western blot 检测磷酸化(p)-PI3K、p-AKT、Bax 和 caspase-3。利用双荧光素酶报告分析和 RNA 下拉分析评估 miR-490-5p 与 circ_0001361 或 IGF2 的相关性。

结果

本研究结果表明,NB 中 circ_0001361 水平升高。circ_0001361 耗竭抑制 NB 细胞的活力,但促进其凋亡。circ_0001361 吸附 miR-490-5p,靶向调节 IGF2。抑制 miR-490-5p 可挽救 circ_0001361 敲低引起的作用,而 IGF2 缺失可挽救 miR-490-5p 抑制剂引起的作用。

结论

总之,circ_0001361 的缺失通过靶向 miR-490-5p/IGF2 轴抑制 NB 进展,提示 circ_0001361 可能是 NB 的一种新的治疗靶点。

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