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通过……的泛素化和降解促进胶质瘤的发展 。（原文此处不完整）

Promotes the Development of Glioma by Ubiquitination and Degradation of .

作者信息

Wei Huaming, Ding Chonglan, Zhuang Huanxia, Hu WeiLi

机构信息

Department of Neurology, Jiyang District People's Hospital of Jinan, Jinan, Shandong 251400, People's Republic of China.

Special Inspection Section, Shandong Zaozhuang Traditional Chinese Medicine Hospital, Zaozhuang, Shandong 277000, People's Republic of China.

出版信息

Onco Targets Ther. 2020 Dec 31;13:13401-13411. doi: 10.2147/OTT.S264459. eCollection 2020.

DOI:10.2147/OTT.S264459
PMID:33408486
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7781021/
Abstract

OBJECTIVE

To investigate the effect of on glioma cells and further explore its underlying molecular mechanisms.

METHODS

Mouse xenograft model was used in this study. The mRNA expression of was detected by qRT-PCR. The cell viability and proliferation activity was detected by MTT assay and colony formation assay. The migration and invasion of glioma cells were determined by Transwell assay. The protein levels of , FOXO1, CyclinD1, C-myc, MMP-2 and TIMP-1 were assessed by Western-blotting. The interaction between TRIM47 and FOXO1 was measured by Co-immunoprecipitation (Co-IP) assay.

RESULTS

In glioma tissues and cells, was significantly up-regulated. Silencing the expression of inhibited the cell viability and proliferation of cells A172 and U251, as well as their ability to invade and migrate. Among them, the expression levels of C-myc and CyclinD1 also decreased, and MMP-2 was down-regulated and TIMP-1 was up-regulated. Similarly, in vivo model, tumor volume and weight also decreased after knockout. Further research showed that TRIM47 inhibited expression by ubiquitination and degradation of , thereby promoting glioma growth and progression.

CONCLUSION

In our study, we confirmed functional role of the axis in the progression of gliomas and provided a potential target for glioma treatment.

摘要

目的

研究[未提及具体物质]对胶质瘤细胞的影响，并进一步探讨其潜在的分子机制。

方法

本研究采用小鼠异种移植模型。通过qRT-PCR检测[未提及具体物质]的mRNA表达。采用MTT法和集落形成试验检测细胞活力和增殖活性。采用Transwell试验测定胶质瘤细胞的迁移和侵袭能力。通过蛋白质印迹法评估[未提及具体物质]、FOXO1、细胞周期蛋白D1、C-myc、基质金属蛋白酶-2（MMP-2）和金属蛋白酶组织抑制因子-1（TIMP-1）的蛋白水平。通过免疫共沉淀（Co-IP）试验检测TRIM47与FOXO1之间的相互作用。

结果

在胶质瘤组织和细胞中，[未提及具体物质]显著上调。沉默[未提及具体物质]的表达可抑制A172和U251细胞的活力和增殖，以及它们的侵袭和迁移能力。其中，C-myc和细胞周期蛋白D1的表达水平也降低，MMP-2下调，TIMP-1上调。同样，在体内模型中，敲除[未提及具体物质]后肿瘤体积和重量也减小。进一步研究表明，TRIM47通过泛素化和降解[未提及具体物质]抑制其表达，从而促进胶质瘤的生长和进展。

结论

在我们的研究中，我们证实了[未提及具体物质]轴在胶质瘤进展中的功能作用，并为胶质瘤治疗提供了一个潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f08d/7781021/e88b2e96b82d/OTT-13-13401-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f08d/7781021/13d89741e749/OTT-13-13401-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f08d/7781021/790d2e1f8b73/OTT-13-13401-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f08d/7781021/c86696f6d7fa/OTT-13-13401-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f08d/7781021/bd621a6dd122/OTT-13-13401-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f08d/7781021/e88b2e96b82d/OTT-13-13401-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f08d/7781021/13d89741e749/OTT-13-13401-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f08d/7781021/790d2e1f8b73/OTT-13-13401-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f08d/7781021/c86696f6d7fa/OTT-13-13401-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f08d/7781021/bd621a6dd122/OTT-13-13401-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f08d/7781021/e88b2e96b82d/OTT-13-13401-g0005.jpg

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