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. 2021 Jun 23;40:205. doi: 10.1186/s13046-021-02015-4

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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. 8 — Schema of CARMN’s role in triple negative breast cancer: Triple negative breast cancer cells have low level of CARMN. CARMN can inhibit breast cancer and sensitize chemotherapy by regulating many essential pathways and processes. CARMN functions partially by producing embedded miR143-3p which binds with MCM5. MCM5 acts as member of DNA replication initiation factor MCM complex, which combines with ORC and licenses DNA replication. Suppressing of MCM5 by CARMN inhibits normal DNA replication, leading to inhibited tumor growth and higher cisplatin sensitivity. Cisplatin can upregulate CARMN to cause cell apoptosis as a feedback. cDDP: cisplatin; ORC: origin recognition complex