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. 2022 Mar 5;22:110. doi: 10.1186/s12935-022-02523-z

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© The Author(s) 2022

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. 1 — MUC1 interacts with several oncogenic pathways like NF-κB. It can activate TGFβ-activated Kinase (TAK) directly and activated NFκB pathway promotes survival and metastasis in BC cells. Besides, MUC1-CD is necessary for TWIST activation and it correlates to overexpression of cyclin D in BC cells. Moreover, MUC1-CD inhibits P53 activity in BC cells, thus it blocks apoptosis in these cells. MUC1-CD has wide range of interactions with different oncogenic and apoptotic molecules. In general, it promotes cell proliferation and resistance to apoptosis in BC cells