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Int. J. Mol. Sci. 2015, 16(9), 21897-21910;

GCN5 Potentiates Glioma Proliferation and Invasion via STAT3 and AKT Signaling Pathways

Department of Pathology, Affiliated Chenggong Hospital, Xiamen University, Xiamen 361000, China
Chinese People's Liberation Army No. 174 Clinical College, Anhui Medical University, Xiamen 361000, China
Department of Oncology, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu 610072, China
These authors contributed equally to this work.
Author to whom correspondence should be addressed.
Academic Editor: Anthony Lemarié
Received: 22 April 2015 / Revised: 27 August 2015 / Accepted: 31 August 2015 / Published: 10 September 2015
(This article belongs to the Section Biochemistry)
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The general control of nucleotide synthesis 5 (GCN5), which is one kind of lysine acetyltransferases, regulates a number of cellular processes, such as cell proliferation, differentiation, cell cycle and DNA damage repair. However, its biological role in human glioma development remains elusive. In the present study, we firstly reported that GCN5 was frequently overexpressed in human glioma tissues and GCN5 was positively correlated with proliferation of cell nuclear antigen PCNA and matrix metallopeptidase MMP9. Meanwhile, down-regulation of GCN5 by siRNA interfering inhibited glioma cell proliferation and invasion. In addition, GCN5 knockdown reduced expression of p-STAT3, p-AKT, PCNA and MMP9 and increased the expression of p21 in glioma cells. In conclusion, GCN5 exhibited critical roles in glioma development by regulating cell proliferation and invasion, which suggested that GCN5 might be a potential molecular target for glioma treatment. View Full-Text
Keywords: GCN5; cell proliferation; cell invasion; STAT3 GCN5; cell proliferation; cell invasion; STAT3

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Liu, K.; Zhang, Q.; Lan, H.; Wang, L.; Mou, P.; Shao, W.; Liu, D.; Yang, W.; Lin, Z.; Lin, Q.; Ji, T. GCN5 Potentiates Glioma Proliferation and Invasion via STAT3 and AKT Signaling Pathways. Int. J. Mol. Sci. 2015, 16, 21897-21910.

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