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Epstein-Barr virus (EBV) actively contributes to the pathological process of nasopharyngeal carcinoma (NPC) by enabling NPC cells to acquire various capacities required for their malignant biological actions. Our earlier works demonstrated that EBV-encoded latent membrane protein 1 (LMP1) enhanced vascular endothelial growth factor (VEGF)-mediated angiogenesis by boosting store-operated Ca 2+ entry (SOCE) upon extracellular epidermal growth factor (EGF) stimulation. However, the antagonistic effects of SOCE blockage on EBV-promoted angiogenesis must be appropriately evaluated in vivo, and the global effect of EBV infection on the EGF-elicited cytosolic Ca 2+ signaling, which regulates VEGF-mediated angiogenesis remains to be further clarified.

cancer management and research

Blockage of store-operated Ca&lt;sup&gt;2+&lt;/sup&gt; entry antagonizes Epstein&amp;ndash;Barr virus-promoted angiogenesis by inhibiting Ca&lt;sup&gt;2+&lt;/sup&gt; signaling-regulated VEGF production in nasopharyngeal carcinoma