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. 2022 Oct 3;13(10):844. doi: 10.1038/s41419-022-05292-9

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© The Author(s) 2022

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — MLN4924 activates MEK1/2-ERK1/2 and MKK4/7-JNK kinases to induce c-FOS and c-JUN, respectively, leading to AP-1 activation. Activated AP-1 then binds to its cis-element in the PD-L1 enhancer sequence to transactivate PD-L1 expression. Accumulated PD-L1 contributes to cancer-associated immune evasion to counteract anti-cancer activity of MLN4924. This process can be inhibited by the inhibitor of MEK1/2 (trametinib), JNK (SP600125) and anti-PD-L1 antibody.