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微小RNA-302e通过靶向血管内皮生长因子A抑制胶质瘤进展。

miR-302e Suppresses Glioma Progression by Targeting VEGFA.

作者信息

Xie Yunpeng, Liu Xin, Hu Tiemin, Wang Weixing

机构信息

Department of Neurosurgery, Chengde Medical College Affiliated Hospital, Chengde, Hebei Province, People's Republic of China.

Department of Oncology, Chengde Medical College Affiliated Hospital, Chengde, Hebei Province, People's Republic of China.

出版信息

Cancer Manag Res. 2020 Oct 30;12:10965-10974. doi: 10.2147/CMAR.S268222. eCollection 2020.

DOI:10.2147/CMAR.S268222
PMID:33154675
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7608593/
Abstract

BACKGROUND

MiRNA can be involved in regulating tumor genesis and development by regulating the expression of specific genes and regulating corresponding signaling pathways. In this study, we explored the function and mechanisms of miR-302e in glioma progression.

METHODS

Experimental methods include the following: real-time quantitative PCR, Western Blot Analysis, CCK8 assay and detection of apoptosis.

RESULTS

MiR-302e was down-regulated in cancer tissues and cell lines, and the expression of miR-302e was negatively correlated with the tumor grade, which indicated poor prognosis in glioma patients. Followed functional analysis showed overexpression of miR-302e inhibited proliferation, migration and invasion but promoted apoptosis of glioma cells, while silencing miR-302e showed the opposite effects. Mechanistic studies have shown that VEGFA was a directed target of miR-302e. Forced expression of VEGFA removed the inhibiting impact of miR-302e on glioma development. In vivo tumorigenesis experiments showed that miR-302e suppressed glioma development by targeting VEGFA.

CONCLUSION

Present study emphasized miR-302e suppressed glioma development by targeting VEGFA, which might be a valuable target for glioma treatment.

摘要

背景

微小RNA（miRNA）可通过调控特定基因的表达以及相应信号通路来参与调节肿瘤的发生和发展。在本研究中，我们探究了miR - 302e在胶质瘤进展中的功能及机制。

方法

实验方法包括以下内容：实时定量聚合酶链反应、蛋白质免疫印迹分析、细胞计数试剂盒8检测以及凋亡检测。

结果

miR - 302e在癌组织和细胞系中表达下调，且miR - 302e的表达与肿瘤分级呈负相关，这表明胶质瘤患者预后较差。随后的功能分析显示，miR - 302e过表达抑制胶质瘤细胞的增殖、迁移和侵袭，但促进其凋亡，而沉默miR - 302e则表现出相反的效果。机制研究表明，血管内皮生长因子A（VEGFA）是miR - 302e的直接靶点。VEGFA的强制表达消除了miR - 302e对胶质瘤发展的抑制作用。体内肿瘤发生实验表明，miR - 302e通过靶向VEGFA抑制胶质瘤发展。

结论

本研究强调miR - 302e通过靶向VEGFA抑制胶质瘤发展，这可能是胶质瘤治疗的一个有价值的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/034445a8139e/CMAR-12-10965-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/bbaf8e4daed7/CMAR-12-10965-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/f8b4a8fae0d9/CMAR-12-10965-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/d3b4586307a7/CMAR-12-10965-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/7bf6903b9cdf/CMAR-12-10965-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/c6c9c07620bb/CMAR-12-10965-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/6e1328554489/CMAR-12-10965-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/a24262cdda6a/CMAR-12-10965-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/034445a8139e/CMAR-12-10965-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/bbaf8e4daed7/CMAR-12-10965-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/f8b4a8fae0d9/CMAR-12-10965-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/d3b4586307a7/CMAR-12-10965-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/7bf6903b9cdf/CMAR-12-10965-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/c6c9c07620bb/CMAR-12-10965-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/6e1328554489/CMAR-12-10965-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/a24262cdda6a/CMAR-12-10965-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91de/7608593/034445a8139e/CMAR-12-10965-g0008.jpg

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