Suppr超能文献

降脂药非诺贝特联合 si-HOTAIR 能有效抑制脑胶质瘤的增殖。

The lipid-lowering drug fenofibrate combined with si-HOTAIR can effectively inhibit the proliferation of gliomas.

机构信息

Department of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University and Institute of Brain and Brain-Inspired Science, Shandong University, Jinan, 250012, Shandong, China.

Key Laboratory of Brain Function Remodeling, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.

出版信息

BMC Cancer. 2021 Jun 3;21(1):664. doi: 10.1186/s12885-021-08417-z.

Abstract

BACKGROUND

Fenofibrate is a fibric acid derivative known to have a lipid-lowering effect. Although fenofibrate-induced peroxisome proliferator-activated receptor alpha (PPARα) transcription activation has been shown to play an important role in the malignant progression of gliomas, the underlying mechanisms are poorly understood.

METHODS

In this study, we analyzed TCGA database and found that there was a significant negative correlation between the long noncoding RNA (lncRNA) HOTAIR and PPARα. Then, we explored the molecular mechanism by which lncRNA HOTAIR regulates PPARα in cell lines in vitro and in a nude mouse glioma model in vivo and explored the effect of the combined application of HOTAIR knockdown and fenofibrate treatment on glioma invasion.

RESULTS

For the first time, it was shown that after knockdown of the expression of HOTAIR in gliomas, the expression of PPARα was significantly upregulated, and the invasion and proliferation ability of gliomas were obviously inhibited. Then, glioma cells were treated with both the PPARα agonist fenofibrate and si-HOTAIR, and the results showed that the proliferation and invasion of glioma cells were significantly inhibited.

CONCLUSIONS

Our results suggest that HOTAIR can negatively regulate the expression of PPARα and that the combination of fenofibrate and si-HOTAIR treatment can significantly inhibit the progression of gliomas. This introduces new ideas for the treatment of gliomas.

摘要

背景

非诺贝特是一种已知具有降脂作用的纤维酸衍生物。虽然非诺贝特诱导的过氧化物酶体增殖物激活受体α(PPARα)转录激活被认为在神经胶质瘤的恶性进展中起重要作用,但潜在机制尚不清楚。

方法

在本研究中,我们分析了 TCGA 数据库,发现长链非编码 RNA(lncRNA)HOTAIR 与 PPARα 之间存在显著的负相关。然后,我们探讨了 lncRNA HOTAIR 在体外细胞系和体内裸鼠神经胶质瘤模型中调节 PPARα 的分子机制,并探讨了 HOTAIR 敲低与非诺贝特联合应用对神经胶质瘤侵袭的影响。

结果

首次表明在神经胶质瘤中敲低 HOTAIR 的表达后,PPARα 的表达明显上调,神经胶质瘤的侵袭和增殖能力明显受到抑制。然后,用 PPARα 激动剂非诺贝特和 si-HOTAIR 处理神经胶质瘤细胞,结果表明神经胶质瘤细胞的增殖和侵袭明显受到抑制。

结论

我们的结果表明 HOTAIR 可以负调控 PPARα 的表达,非诺贝特和 si-HOTAIR 联合治疗可以显著抑制神经胶质瘤的进展。这为神经胶质瘤的治疗提供了新的思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a0b/8173837/bdc71b2e60a7/12885_2021_8417_Fig1_HTML.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