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微小RNA-17和微小RNA-93通过靶向脊索瘤患者中的p21促进肿瘤进展。

MiR-17 and miR-93 Promote Tumor Progression by Targeting p21 in Patients with Chordoma.

作者信息

Dong Wei, Li Jingwu, Dong Xiaoliu, Shi Wenjian, Zhang Yu, Liu Yongliang

机构信息

Department of Neurosurgery, Tangshan People's Hospital, Tangshan, Hebei, People's Republic of China.

Department of Tumor Surgery, Tangshan People's Hospital, Tangshan, Hebei, People's Republic of China.

出版信息

Onco Targets Ther. 2021 May 12;14:3109-3118. doi: 10.2147/OTT.S307138. eCollection 2021.

DOI:10.2147/OTT.S307138
PMID:34054299
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8153071/
Abstract

OBJECTIVE

MicroRNAs have been implicated in the progression of various cancers. However, the role of microRNAs in chordoma remains to be further elucidated. Here, we purposed to character the role of two microRNAs, miR-17 and miR-93, and their potential mechanisms in chordoma.

METHODS

The expression and prognostic value of miR-17 and miR-93 were assessed by the quantitative real-time polymerase chain reaction, Kaplan-Meier survival curve, and Cox regression analysis. The effects of miR-17/93 mimics on chordoma cell proliferation, colony formation, and invasion were analyzed by CCK-8 assay, colony formation assay, and transwell assay. The downstream target of miR-17/93 was further explored via luciferase reporter assay.

RESULTS

High expression of miR-17/93 was identified in chordoma tissues, and was associated with poor prognosis. Overexpression of miR-17/93 contributed to cell proliferation, colony formation, and invasion. Mechanistically, we demonstrated that miR-17/93 directly targeted p21 and decreased the expression of p21. Besides, the rescue assay further confirmed the essential role of the miR-17/93-p21 axis in chordoma.

CONCLUSION

Our results revealed the potential oncogenic effect of the miR-17/93 on chordoma progression, and suggested that the miR-17/93-p21 axis served as a promising therapeutic target in chordoma.

摘要

目的

微小RNA已被证明与多种癌症的进展有关。然而，微小RNA在脊索瘤中的作用仍有待进一步阐明。在此，我们旨在研究两种微小RNA，即miR-17和miR-93在脊索瘤中的作用及其潜在机制。

方法

通过定量实时聚合酶链反应、Kaplan-Meier生存曲线和Cox回归分析评估miR-17和miR-93的表达及预后价值。通过CCK-8检测、集落形成检测和Transwell检测分析miR-17/93模拟物对脊索瘤细胞增殖、集落形成和侵袭的影响。通过荧光素酶报告基因检测进一步探索miR-17/93的下游靶点。

结果

在脊索瘤组织中鉴定出miR-17/93的高表达，且与预后不良相关。miR-17/93的过表达促进细胞增殖、集落形成和侵袭。机制上，我们证明miR-17/93直接靶向p21并降低p21的表达。此外，挽救实验进一步证实了miR-17/93-p21轴在脊索瘤中的重要作用。

结论

我们的结果揭示了miR-17/93对脊索瘤进展的潜在致癌作用，并表明miR-17/93-p21轴是脊索瘤中一个有前景的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41d0/8153071/f3d60b8ecbdd/OTT-14-3109-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41d0/8153071/ec1f5a23660f/OTT-14-3109-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41d0/8153071/aa3153d422f4/OTT-14-3109-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41d0/8153071/fd9cc56f381d/OTT-14-3109-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41d0/8153071/f3d60b8ecbdd/OTT-14-3109-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41d0/8153071/ec1f5a23660f/OTT-14-3109-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41d0/8153071/aa3153d422f4/OTT-14-3109-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41d0/8153071/fd9cc56f381d/OTT-14-3109-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41d0/8153071/f3d60b8ecbdd/OTT-14-3109-g0004.jpg

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