Tumor cells meet the drastic energy requirements for cell survival and
unlimited proliferation through metabolic reprogramming, and one of the
important aspects of metabolic reprogramming is changes in lipid
metabolism. Increasing evidence suggests that, like tumor cells in
general, host cells infected with onco-viruses significantly alter
metabolic requirements and generate substances for viral replication and
virion production by altering the metabolism of host cells. HPV, EBV and
KSHV are the three important contributors to virus-related tumors that
appear in people before the age of 50. On the basis of reviewing the
changes of lipid metabolism in tumor cells, this review summarizes the
interesting association between HPV, EBV or KSHV and lipid metabolism
from these three major tumor viruses in order to provide new insight
into the treatment of virus-related tumors.
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.
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