Epstein-Barr virus Latent Membrane Protein LMP1 reduces p53 protein levels independent of the PI3K-Akt pathway

BMC Research Notes

Alan Soo-Beng Khoo¹  Munirah Ahmad¹  Roslina Husaini¹ 

[1] Molecular Pathology Unit, Cancer Research Centre, Institute for Medical Research, Jalan Pahang, 50588 Kuala Lumpur, Malaysia

关键词: Nasopharyngeal carcinoma (NPC), Epstein-Barr virus, Latent membrane protein, p53 tumour suppressor gene, ubiquitination;   

Others  :  1166858
DOI  :  10.1186/1756-0500-4-551

 received in 2011-08-19, accepted in 2011-12-21,  发布年份 2011

【 摘 要 】

Background

Nasopharyngeal carcinoma (NPC) is an epithelial malignancy, which commonly occurs in Southern China, Taiwan, North Africa and Southeast Asia. Nasopharyngeal carcinoma is strongly associated with Epstein-Barr virus infection. The p53 tumour suppressor protein is rarely mutated in NPC suggesting that the inactivation of p53 pathway in NPC could be due to the presence of EBV proteins. The aim of this work was to determine the effects of EBV proteins namely LMP1 and LMP2A on the expression levels of p53 protein.

Findings

In this work we found that LMP1, but not LMP2A, decreased p53 protein levels. Overexpression of LMP1 resulted in increased ubiquitination of p53 suggesting that the decreased p53 protein levels by LMP1 was due to increased degradation of the protein. The reduction of p53 protein levels was independent of the PI3K-Akt pathway.

Conclusions

LMP1, but not LMP2A, reduced p53 protein levels through the increase in the polyubiquitination of p53 protein and was independent of the PI3K-Akt pathway.

【 授权许可】

   
2011 Khoo et al; licensee BioMed Central Ltd.

【 图 表 】

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