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BioMed Research International
Volume 2018, Article ID 8591397, 12 pages
https://doi.org/10.1155/2018/8591397
Research Article

Involvement of P2X7 Receptor in Proliferation and Migration of Human Glioma Cells

1Department of Neurosurgery, The First Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China
2Department of Head and Neck Surgery, Affiliated Tumor Hospital of Nantong University, Nantong 226001, China
3Department of Ophthalmology, Affiliated Hospital of Nantong University, Nantong 226001, China
4Schepens Eye Research Institute, Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA

Correspondence should be addressed to Min Ji; moc.liamtoh@4321ijyma and Yongping You; nc.ude.umjn@9lpyy

Received 5 September 2017; Revised 22 November 2017; Accepted 29 November 2017; Published 9 January 2018

Academic Editor: Jens Schittenhelm

Copyright © 2018 Zhenhua Ji et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Previous studies have demonstrated that activation of P2X7 receptors (P2X7R) results in the proliferation and migration of some types of tumor. Here, we asked whether and how the activated P2X7R contribute to proliferation and migration of human glioma cells. Results showed that the number of P2X7R positive cells was increasing with grade of tumor. In U87 and U251 human glioma cell lines, both expressed P2X7R and the expression was enhanced by 3′-O-(4-benzoylbenzoyl) ATP (BzATP), the agonist of P2X7R, and siRNA. Our results also showed that 10 μM BzATP was sufficient to induce the proliferation of glioma cell significantly, while the cell proliferation reached the peak with 100 μM BzATP. Also, the migration of U87 and U251 cells was significantly increased upon BzATP treatment. However, the number of apoptotic cells of U87 and U251 was not significantly changed by BzATP. In addition, the expression of ERK, p-ERK, and proliferating cell nuclear antigen (PCNA) protein was increased in BzATP-treated U87 and U251 glioma cells. PD98059, an inhibitor of the MEK/ERK pathway, blocked the increased proliferation and migration of glioma cells activated by BzATP. These results suggest that ERK pathway is involved in the proliferation and migration of glioma cells induced by P2X7R activation.