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. 2022 Feb 23;13(2):174. doi: 10.1038/s41419-022-04624-z

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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. 6 — (Left) SAPCD2 binds to E2F7 in the cytoplasm and thereby alters the subcellular distribution of E2F7, derepressing E2F signaling transactivation, and promoting NB progression. XPO1 mediates the nuclear export of E2F7 in NB cells. (Right) GSK-J4 treatment reduces the level of SAPCD2 in NB cells and limits the binding of SAPCD2 to E2F7 in the cytoplasm. Selinexor inhibits the XPO1-dependent nuclear export of E2F7. Nuclear accumulation of E2F7 inhibits the E2F signaling and suppresses the progression of NB cells.