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Original Research Article | OPEN ACCESS

MiR-455-3p regulates glioma cell proliferation by targeting PAX6

Jizhong Han, Yu Xiong, Huajiang Deng, Jie Zhou, Lilei Peng, Wei Xiang, Yang Ming, Ligang Chen

Department of Neurosurgery, Affiliated Hospital of Southwest Medical University, No. 25 Taiping Street, Jiangyang District, Luzhou, Sichuan 646000, China;

For correspondence:-  Ligang Chen   Email: chenligangllg@163.com   Tel:+868303165461

Accepted: 27 March 2019        Published: 30 April 2019

Citation: Han J, Xiong Y, Deng H, Zhou J, Peng L, Xiang W, et al. MiR-455-3p regulates glioma cell proliferation by targeting PAX6. Trop J Pharm Res 2019; 18(4):689-695 doi: 10.4314/tjpr.v18i4.2

© 2019 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the role of miR-455-3p in gliomas.
Method: Quantitative real-time polymerase chain reaction was used to measure miR-455-3p and paired box 6 (PAX6) levels in glioma cell lines. Western blot analysis was used to determine the expression of cell cycle regulators. In addition to over-expression, silencing of miR-455-3p or PAX6 was performed to study the functions of miR-455-3p in gliomas.
Results: The levels of miR-455-3p were significantly up-regulated in glioma cell lines (p < 0.05), while miR-455-3p over-expression increased glioma cell proliferation and interfered with the progress of the cell cycle (p < 0.01). Furthermore, endogenous miR-455-3p silencing prevented glioma cell proliferation by regulating cell cycle progression (p < 0.05).The results also showed that PAX6 controlled the cell cycle while PAX6 silencing selectively regulated p21 expression (p < 0.01). Furthermore, miR-455-3p and PAX6 influenced p53 expression. Re-introduction of PAX6 expressing vector into glioma cells rescued the pro-tumoral effect of miR-455-3p overexpression.
Conclusion: These findings demonstrate the role of miR-455-3p as a tumour oncogene in gliomas via regulation of the cell cycle, indicating that miR-455-3p might act as a new treatment strategy for glioma cell tumours and a predictor of survival in glioma patients.

Keywords: Glioma; Endogenous miR-455-3p, PAX6, Therapeutic target

Impact Factor
Thompson Reuters (ISI): 0.6 (2023)
H-5 index (Google Scholar): 49 (2023)

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