Suppr超能文献

敲低circ-TTBK2通过调控miR-1283和CHD1抑制胶质瘤进展。

Knockdown of circ-TTBK2 Inhibits Glioma Progression by Regulating miR-1283 and CHD1.

作者信息

Han Chengchen, Wang Shuwei, Wang Hongwei, Zhang Jianning

机构信息

Department of Neurosurgery, The Sixth Medical Center of PLA General Hospital, Beijing 100048, People's Republic of China.

出版信息

Cancer Manag Res. 2020 Oct 13;12:10055-10065. doi: 10.2147/CMAR.S252916. eCollection 2020.

Abstract

BACKGROUND

Dysregulated circular RNAs (circRNAs) are involved in the development of glioma. This paper aims to analyze the role and mechanism of circRNA tau tubulin kinase 2 (circ-TTBK2) in glioma progression.

METHODS

The glioma samples and normal brain tissues were collected. The levels of circ-TTBK2, microRNA-1283 (miR-1283) and chromodomain helicase DNA-binding protein 1 (CHD1) were examined via quantitative reverse transcription polymerase chain reaction or Western blot. Cell proliferation, migration, invasion and glycolysis were determined via 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide, transwell assay, Western blot, glucose and lactate assay kits. The target relationship was analyzed via dual-luciferase reporter assay. The xenograft model was established using U251 cells.

RESULTS

circ-TTBK2 expression was increased in glioma tissues and cells. circ-TTBK2 knockdown suppressed glioma cell proliferation, migration, invasion and glycolysis. circ-TTBK2 was a sponge for miR-1283, and knockdown of miR-1283 reversed the effect of circ-TTBK2 silence on glioma progression. CHD1 was targeted via miR-1283, and miR-1283 repressed glioma cell proliferation, migration, invasion and glycolysis via decreasing CHD1. Knockdown of circ-TTBK2-reduced CHD1 expression by mediating miR-1283. Silence of circ-TTBK2 reduced xenograft tumor growth.

CONCLUSION

Down-regulation of circ-TTBK2 suppressed glioma development by regulating miR-1283 and CHD1, providing a new mechanism for understanding glioma pathogenesis.

摘要

背景

环状RNA(circRNAs)失调参与胶质瘤的发生发展。本文旨在分析环状微管蛋白激酶2(circ-TTBK2)在胶质瘤进展中的作用及机制。

方法

收集胶质瘤样本和正常脑组织。通过定量逆转录聚合酶链反应或蛋白质免疫印迹法检测circ-TTBK2、微小RNA-1283(miR-1283)和染色质结构域解旋酶DNA结合蛋白1(CHD1)的水平。通过3-(4,5-二甲基-2-噻唑基)-2,5-二苯基-2-H-四氮唑溴盐、Transwell实验、蛋白质免疫印迹法、葡萄糖和乳酸检测试剂盒测定细胞增殖、迁移、侵袭和糖酵解。通过双荧光素酶报告基因实验分析靶标关系。使用U251细胞建立异种移植模型。

结果

circ-TTBK2在胶质瘤组织和细胞中表达升高。circ-TTBK2敲低抑制胶质瘤细胞增殖、迁移、侵袭和糖酵解。circ-TTBK2是miR-1283的海绵,miR-1283敲低可逆转circ-TTBK2沉默对胶质瘤进展的影响。CHD1是miR-1283的靶标,miR-1283通过降低CHD1抑制胶质瘤细胞增殖、迁移、侵袭和糖酵解。circ-TTBK2敲低通过介导miR-1283降低CHD1表达。circ-TTBK2沉默减少异种移植瘤生长。

结论

circ-TTBK2的下调通过调节miR-1283和CHD1抑制胶质瘤发展,为理解胶质瘤发病机制提供了新机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/660f/7568596/0b6b680a21b4/CMAR-12-10055-g0001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验