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Open Access Highly Accessed Research article

Meta-analysis of nasopharyngeal carcinoma microarray data explores mechanism of EBV-regulated neoplastic transformation

Xia Chen12, Shuang Liang1, WenLing Zheng13, ZhiJun Liao1, Tao Shang1 and WenLi Ma1*

Author Affiliations

1 Institute of Genetic Engineering, Southern Medical University, Guangzhou, PR China

2 Xiangya Pingkuang associated hospital, Pingxiang, Jiangxi, PR China

3 Southern Genomics Research Center, Guangzhou, Guangdong, PR China

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BMC Genomics 2008, 9:322  doi:10.1186/1471-2164-9-322

Published: 7 July 2008

Abstract

Background

Epstein-Barr virus (EBV) presumably plays an important role in the pathogenesis of nasopharyngeal carcinoma (NPC), but the molecular mechanism of EBV-dependent neoplastic transformation is not well understood. The combination of bioinformatics with evidences from biological experiments paved a new way to gain more insights into the molecular mechanism of cancer.

Results

We profiled gene expression using a meta-analysis approach. Two sets of meta-genes were obtained. Meta-A genes were identified by finding those commonly activated/deactivated upon EBV infection/reactivation. These genes could be key players for pathways de-regulated by EBV during latent infection and lytic proliferation. Meta-B genes were obtained from differential genes commonly expressed in NPC and PEL (primary effusion lymphoma). We then integrated meta-A, meta-B and associated factors into an interaction network using acquired information. Our analysis suggests that NPC transformation depends on timely regulation of DEK, CDK inhibitor(s), p53, RB and several transcriptional cascades, interconnected by E2F, AP-1, NF-κB, STAT3 among others during latent and lytic cycles.

Conclusion

In conclusion, our meta-analysis strategy re-analyzed EBV-related tumor data sets and identified sets of meta-genes possibly involved in maintaining latent or switching to lytic cycles of EBV in NPC. The results of this analysis may shed new lights to further our understanding of the EBV-led neoplastic transformation.