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Int. J. Mol. Sci. 2016, 17(11), 1859; doi:10.3390/ijms17111859

Low Expression of CAPON in Glioma Contributes to Cell Proliferation via the Akt Signaling Pathway

1
Institute of Nervous System Diseases, Xuzhou Medical University, 84 West Huai-Hai Road, Xuzhou 221002, Jiangsu, China
2
Brain Hospital, Affiliated Hospital of Xuzhou Medical University, 99 West Huai-Hai Road, Xuzhou 221002, Jiangsu, China
3
People’s Hospital of Juxian, 100 Fulaizhong Road in Juxian, Rizhao 276500, Shandong, China
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Academic Editor: William Chi-shing Cho
Received: 22 August 2016 / Revised: 27 October 2016 / Accepted: 1 November 2016 / Published: 18 November 2016
(This article belongs to the Collection Advances in Molecular Oncology)
View Full-Text   |   Download PDF [5680 KB, uploaded 18 November 2016]   |  

Abstract

CAPON is an adapter protein for nitric oxide synthase 1 (NOS1). CAPON has two isoforms in the human brain: CAPON-L (long form of CAPON) and CAPON-S (short form of CAPON). Recent studies have indicated the involvement of CAPON in tumorigenesis beyond its classical role in NOS1 activity regulation. In this study, we found that the protein levels of CAPON-S, but not than CAPON-L, were significantly decreased in glioma tissues. Therefore, we established lentivirus-mediated stable cell lines with CAPON-S overexpression or down-regulation, and investigated the role of CAPON-S in the proliferation of glioma cells by using CCK8, EdU, and flow cytometry assays. Overexpression of CAPON-S reduced the cell variability and the percentage of EdU-positive cells, and arrested the cells in the G1 phase in glioma cells. Silencing of CAPON by short-hairpin RNA showed the opposite effects. Furthermore, an intracellular signaling array revealed that overexpression of CAPON-S resulted in a remarkable reduction in the phosphorylation of Akt and S6 ribosomal protein in glioma cells, which was further confirmed by Western blot. These findings suggest that CAPON may function as a tumor suppressor in human brain glioma and that the inactivation of the Akt signaling pathway caused by CAPON-S overexpression may provide insight into the underlying mechanism of CAPON in glioma cell proliferation. View Full-Text
Keywords: CAPON; glioma; proliferation; Akt; mTOR CAPON; glioma; proliferation; Akt; mTOR
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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. (CC BY 4.0).

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Gao, S.; Wang, J.; Zhang, T.; Liu, G.; Jin, L.; Ji, D.; Wang, P.; Meng, Q.; Zhu, Y.; Yu, R. Low Expression of CAPON in Glioma Contributes to Cell Proliferation via the Akt Signaling Pathway. Int. J. Mol. Sci. 2016, 17, 1859.

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