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

Abstract

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.

• Authors: Kun Liu, Qing Zhang, Haitao Lan, Liping Wang, Pengfei Mou, Wei Shao, Dan Liu, Wensheng Yang, Zhen Lin, Qingyuan Lin, Tianhai Ji
• Journal: International journal of molecular sciences (Int J Mol Sci) Vol. 16 Issue 9 Pg. 21897-910 (Sep 10 2015) ISSN: 1422-0067 [Electronic] Switzerland
• PMID: 26378521 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Proliferating Cell Nuclear Antigen
• STAT3 Transcription Factor
• p300-CBP Transcription Factors
• p300-CBP-associated factor
• Proto-Oncogene Proteins c-akt
• Matrix Metalloproteinase 9

Topics

• Brain Neoplasms (genetics, metabolism, pathology)
• Cell Cycle (genetics)
• Cell Line, Tumor
• Cell Movement (genetics)
• Cell Proliferation
• Gene Expression
• Gene Knockdown Techniques
• Gene Silencing
• Glioma (genetics, metabolism, pathology)
• Humans
• Immunohistochemistry
• Matrix Metalloproteinase 9 (genetics, metabolism)
• Proliferating Cell Nuclear Antigen (genetics, metabolism)
• Proto-Oncogene Proteins c-akt (metabolism)
• STAT3 Transcription Factor (metabolism)
• Signal Transduction
• p300-CBP Transcription Factors (genetics, metabolism)