Back to Search
Start Over
GCN5 Potentiates Glioma Proliferation and Invasion via STAT3 and AKT Signaling Pathways.
- Source :
-
International journal of molecular sciences [Int J Mol Sci] 2015 Sep 10; Vol. 16 (9), pp. 21897-910. Date of Electronic Publication: 2015 Sep 10. - Publication Year :
- 2015
-
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.
- Subjects :
- Brain Neoplasms genetics
Brain Neoplasms pathology
Cell Cycle genetics
Cell Line, Tumor
Cell Movement genetics
Cell Proliferation
Gene Expression
Gene Knockdown Techniques
Gene Silencing
Glioma genetics
Glioma pathology
Humans
Immunohistochemistry
Matrix Metalloproteinase 9 genetics
Matrix Metalloproteinase 9 metabolism
Proliferating Cell Nuclear Antigen genetics
Proliferating Cell Nuclear Antigen metabolism
p300-CBP Transcription Factors genetics
Brain Neoplasms metabolism
Glioma metabolism
Proto-Oncogene Proteins c-akt metabolism
STAT3 Transcription Factor metabolism
Signal Transduction
p300-CBP Transcription Factors metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1422-0067
- Volume :
- 16
- Issue :
- 9
- Database :
- MEDLINE
- Journal :
- International journal of molecular sciences
- Publication Type :
- Academic Journal
- Accession number :
- 26378521
- Full Text :
- https://doi.org/10.3390/ijms160921897