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. 2024 Aug 30;14:20191. doi: 10.1038/s41598-024-71059-1

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 1 — Effects of EIF4 protein family on breast cancer cells and its pathway regulation mechanism. An activated S6K1-PDCD4 pathway promotes the unwinding of EIF4A, and the 4EBP-EIF4E pathway accelerates the release of activated EIF4E, which together promote the formation of the EIF4E complex and increase the abundance of MUC1-C oncoprotein in breast cancer. MUC1-C oncoprotein and activated EIF4E promote tumorigenesis, tumor cell metastasis, cancer cell angiogenesis and vascular invasion.