Abstract
Previous studies have indicated that Epstein-Barr virus (EBV) can modulate the Wnt pathway in virus-infected cells and this effect is mediated by EBV-encoded oncogene latent membrane protein 1 (LMP1). Here we have reassessed the role of LMP1 in regulating the expression of various mediators of the canonical Wnt cascade. Contradicting the previous finding, we found that the levels of E-cadherin, β-catenin, Glycogen Synthase Kinase 3ß (GSK3β), axin and α-catenin were not affected by the expression of LMP1 sequences from normal B cells or nasopharyngeal carcinoma. Moreover, we also show that LMP1 expression had no detectable effect on the E-cadherin and β-catenin interaction and did not induce transcriptional activation of β-catenin. Taken together these studies demonstrate that EBV-mediated activation of Wnt pathway is not dependent on the expression of LMP1.
Highlights
The oncogenic potential of Epstein-Barr virus (EBV) is well recognized, and the virus is associated with a number of human malignancies, including Burkitt’s lymphoma (BL) and nasopharyngeal carcinoma (NPC) [1]
latent membrane protein 1 (LMP1) sequences from both normal B cells or from NPC showed no effect on the expression of E-cadherin and b-catenin
To ensure that the results described above were not influenced by the covalent linking of LMP1 with EGFP, we expressed LMP1 protein in HaCaT cells without EGFP and assessed the expression of b-catenin
Summary
The oncogenic potential of Epstein-Barr virus (EBV) is well recognized, and the virus is associated with a number of human malignancies, including Burkitt’s lymphoma (BL) and nasopharyngeal carcinoma (NPC) [1]. We show that transient or stable expression of LMP1 sequences from normal B cells and NPC does not impair the expression of E-Cadherin and other mediators of the Wnt pathway. We demonstrate that LMP1 expression in human cells had minimal effect on the interaction of E-cadherin and b-catenin no evidence of b-catenin-mediated transcriptional activation was observed.
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