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Published in: Journal of Experimental & Clinical Cancer Research 1/2010

Open Access 01-12-2010 | Research

Overexpression of candidate tumor suppressor ECRG4 inhibits glioma proliferation and invasion

Authors: Wei Li, Xinrui Liu, Bo Zhang, Dongxue Qi, Lihong Zhang, Yuhong Jin, Hongfa Yang

Published in: Journal of Experimental & Clinical Cancer Research | Issue 1/2010

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Abstract

Background

ECRG4 has been shown to be a candidate tumor suppressor in several tumors, but its role in glioma remains poorly understood. In this study, we examined the mRNA expression of ECRG4 and investigated its biological role in glioma cells.

Methods

Real-time PCR was used to examine expression of ECRG4 in gliomas and their matched brain tissues. The effect of ECRG4 expression on cell proliferation, invasion, and migration was investigated in human U251 glioma cells. Finally, the regulation of transcription factor NF-kB by ECRG4 was evaluated by western blotting.

Results

Of the 10 paired samples analyzed, 9 glioma tissues displayed the decreased expression of ECRG4 compared to matched normal brain tissues. Cells transfected with ECRG4 showed significantly decreased cell proliferation as evaluated by MTT and colony formation assays. Furthermore, overexpression inhibited cell migration and invasion in transwell and Boyden chamber experiments and retarded the cell cycle progression from G1 to S phase by FACSCaliber cytometry. Protein levels of nuclear transcription factor NF-kB, which is involved in cell proliferation, inversely correlated with ECRG4 expression.

Conclusion

Our data suggest that ECRG4 serves as a tumor suppressor in glioma.
Appendix
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Metadata
Title
Overexpression of candidate tumor suppressor ECRG4 inhibits glioma proliferation and invasion
Authors
Wei Li
Xinrui Liu
Bo Zhang
Dongxue Qi
Lihong Zhang
Yuhong Jin
Hongfa Yang
Publication date
01-12-2010
Publisher
BioMed Central
Published in
Journal of Experimental & Clinical Cancer Research / Issue 1/2010
Electronic ISSN: 1756-9966
DOI
https://doi.org/10.1186/1756-9966-29-89

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