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. 2021 Feb 6;21:93. doi: 10.1186/s12935-021-01793-3

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — EBV-induced oncogenesis through the Wnt/β-catenin signaling pathway. The binding of Wnt and Frizzled protein will prompt LRP to phosphorylate and recruit protein complexes, and then these protein complexes will dissociate to release stable expression of β-catenin. Free β-catenin binds to TCF to activate the corresponding transcription after entering the nucleus. LMP2A inhibits the expression of GSK-3β through the PI3K/AKT signaling pathway, which interferes with the formation of protein complexes and promotes the accumulation of β-catenin in the nucleus to induce EMT. WTX can inhibit the expression of β-catenin, and LMP1 in transgenic mice will interfere with the inhibitory effect of WTX, resulting in the stable expression of β-catenin and leading to dysplasia