LMP1 encoded by Epstein-Barr virus may activate AHR through the ERK pathway in nasopharyngeal carcinoma cells

Aim: To investigate the role of AHR in nasopharyngeal carcinoma (NPC) and explore the relationship between Epstein-Barr virus (EBV) infection and the AHR pathway. Methods: The effect of LMP1 on the expression of AHR was analyzed using real-time PCR and western blot. Proliferation and migration of cells were assessed using CCK8 and Transwell analysis. Results: EBV infection downregulated the expression of AHR in NPC cells, possibly through activation of the ERK pathway by LMP1 thereby accelerating AHR proteasomal degradation following translocation to the nucleus. Cell proliferation, migration and autophagy are promoted by activating the AHR pathway. Conclusion: In NPC cells, LMP1 increases the phosphorylation of ERK, which may activate the AHR pathway. Plain language summary What is this article about?This article describes the role of a virus, the Epstein-Barr virus (EBV), in the development of a type of cancer that affects the throat called nasopharyngeal carcinoma (NPC). One of the proteins made by the virus, called latent membrane protein 1 (LMP1), is thought to play a role in the development of NPC. We investigate how LMP1 may cause NPC. What were the results?We found that LMP1 was linked to higher levels of two genes, CYP1A1 and CYP1B1, which are targets of a receptor called the aryl hydrocarbon receptor (AHR). This may be linked to the movement of AHR to the cell's control center, where it can play a role in the development of cancer. What do the results of the study mean?This article suggests a pathway for how EBV may cause NPC.