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

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...

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Autores principales: Gao, Shangfeng, Wang, Jie, Zhang, Tong, Liu, Guangping, Jin, Lei, Ji, Daofei, Wang, Peng, Meng, Qingming, Zhu, Yufu, Yu, Rutong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5133859/
https://www.ncbi.nlm.nih.gov/pubmed/27869735
http://dx.doi.org/10.3390/ijms17111859
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author Gao, Shangfeng
Wang, Jie
Zhang, Tong
Liu, Guangping
Jin, Lei
Ji, Daofei
Wang, Peng
Meng, Qingming
Zhu, Yufu
Yu, Rutong
author_facet Gao, Shangfeng
Wang, Jie
Zhang, Tong
Liu, Guangping
Jin, Lei
Ji, Daofei
Wang, Peng
Meng, Qingming
Zhu, Yufu
Yu, Rutong
author_sort Gao, Shangfeng
collection PubMed
description 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.
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spelling pubmed-51338592016-12-12 Low Expression of CAPON in Glioma Contributes to Cell Proliferation via the Akt Signaling Pathway Gao, Shangfeng Wang, Jie Zhang, Tong Liu, Guangping Jin, Lei Ji, Daofei Wang, Peng Meng, Qingming Zhu, Yufu Yu, Rutong Int J Mol Sci Article 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. MDPI 2016-11-18 /pmc/articles/PMC5133859/ /pubmed/27869735 http://dx.doi.org/10.3390/ijms17111859 Text en © 2016 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Gao, Shangfeng
Wang, Jie
Zhang, Tong
Liu, Guangping
Jin, Lei
Ji, Daofei
Wang, Peng
Meng, Qingming
Zhu, Yufu
Yu, Rutong
Low Expression of CAPON in Glioma Contributes to Cell Proliferation via the Akt Signaling Pathway
title Low Expression of CAPON in Glioma Contributes to Cell Proliferation via the Akt Signaling Pathway
title_full Low Expression of CAPON in Glioma Contributes to Cell Proliferation via the Akt Signaling Pathway
title_fullStr Low Expression of CAPON in Glioma Contributes to Cell Proliferation via the Akt Signaling Pathway
title_full_unstemmed Low Expression of CAPON in Glioma Contributes to Cell Proliferation via the Akt Signaling Pathway
title_short Low Expression of CAPON in Glioma Contributes to Cell Proliferation via the Akt Signaling Pathway
title_sort low expression of capon in glioma contributes to cell proliferation via the akt signaling pathway
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5133859/
https://www.ncbi.nlm.nih.gov/pubmed/27869735
http://dx.doi.org/10.3390/ijms17111859
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