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微小RNA-181b通过抑制SP1介导的葡萄糖代谢来抑制多形性胶质母细胞瘤的生长。

MiR-181b suppress glioblastoma multiforme growth through inhibition of SP1-mediated glucose metabolism.

作者信息

Yin JianXing, Shi ZhuMei, Wei WenJin, Lu Chenfei, Wei Yutian, Yan Wei, Li Rui, Zhang JunXia, You YongPing, Wang XieFeng

机构信息

1Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.

2Department of Neurosurgery, The Affiliated Ganzhou Hospital of Nanchang University, 16 Meiguan Avenue, Ganzhou, 341000 Jiangxi China.

出版信息

Cancer Cell Int. 2020 Mar 4;20:69. doi: 10.1186/s12935-020-1149-7. eCollection 2020.

DOI:10.1186/s12935-020-1149-7
PMID:32158359
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7057587/
Abstract

BACKGROUND

Glucose metabolic reprogramming is a significant hallmark of malignant tumors including GBM. Previous studies suggest that microRNAs play key roles in modulating this process in GBM cells. miR-181b acts as a tumor suppressor miRNA in influencing glioma tumorigenesis. Our previous results showed that miR-181b was down-regulated in glioma cells and tissues.

METHODS

The extracellular acidification rate (ECAR), colony formation assay and levels of Glut1 and PKM2 were measured to assess the glucose metabolic and proliferation changes in GBM cells overexpressing miR-181b. Immunoblotting and luciferase reporter assay were performed to confirm the expression and role of SP1 as a direct target of miR-181b. ChIP assay was used to figure out the transcriptional regulation of SP1 on Glut1 and PKM2. In vivo study was examined for the role of miR-181b in GBM cells.

RESULTS

MiR-181b overexpression significantly reduced the glucose metabolic and colony formation ability of GBM cells. And, SP1 was confirmed as a direct target of miR-181b while upregulation of SP1 could reverse the influence of overexpression of miR-181b. Furthermore, Glut1 and PKM2 could be regulated by SP1. Finally, miR-181b could inhibit the tumor growth in vivo.

CONCLUSIONS

Our article demonstrated the inhibitory effect of miR-181b on glucose metabolism and proliferation in GBM by suppressing SP1 expression.

摘要

背景

葡萄糖代谢重编程是包括胶质母细胞瘤（GBM）在内的恶性肿瘤的一个重要特征。先前的研究表明，微小RNA在调节GBM细胞的这一过程中起关键作用。miR-181b在影响胶质瘤发生过程中作为一种肿瘤抑制性微小RNA发挥作用。我们之前的结果显示，miR-181b在胶质瘤细胞和组织中表达下调。

方法

测量细胞外酸化率（ECAR）、集落形成试验以及Glut1和PKM2的水平，以评估过表达miR-181b的GBM细胞中葡萄糖代谢和增殖的变化。进行免疫印迹和荧光素酶报告基因检测，以确认SP1作为miR-181b直接靶点的表达及作用。采用染色质免疫沉淀试验（ChIP）来确定SP1对Glut1和PKM2的转录调控。在体内研究中检测miR-181b在GBM细胞中的作用。

结果

miR-181b过表达显著降低了GBM细胞的葡萄糖代谢和集落形成能力。并且，SP1被确认为miR-181b的直接靶点，而SP1的上调可逆转miR-181b过表达的影响。此外，Glut1和PKM2可受SP1调控。最后，miR-181b可在体内抑制肿瘤生长。

结论

我们的文章证明了miR-181b通过抑制SP1表达对GBM的葡萄糖代谢和增殖具有抑制作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec7e/7057587/a4230ad87c3a/12935_2020_1149_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec7e/7057587/c11ecd267856/12935_2020_1149_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec7e/7057587/8b9bf5b940d6/12935_2020_1149_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec7e/7057587/9d502c97829b/12935_2020_1149_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec7e/7057587/1dac754eecf9/12935_2020_1149_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec7e/7057587/113b8fd4c204/12935_2020_1149_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec7e/7057587/e3e67442abb4/12935_2020_1149_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec7e/7057587/a4230ad87c3a/12935_2020_1149_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec7e/7057587/c11ecd267856/12935_2020_1149_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec7e/7057587/8b9bf5b940d6/12935_2020_1149_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec7e/7057587/9d502c97829b/12935_2020_1149_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec7e/7057587/1dac754eecf9/12935_2020_1149_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec7e/7057587/113b8fd4c204/12935_2020_1149_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec7e/7057587/e3e67442abb4/12935_2020_1149_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec7e/7057587/a4230ad87c3a/12935_2020_1149_Fig7_HTML.jpg

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