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. 2024 Sep 16;25(10):4153–4167. doi: 10.1038/s44319-024-00260-0

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© The Author(s) 2024

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 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/. Creative Commons Public Domain Dedication waiver http://creativecommons.org/publicdomain/zero/1.0/ applies to the data associated with this article, unless otherwise stated in a credit line to the data, but does not extend to the graphical or creative elements of illustrations, charts, or figures. This waiver removes legal barriers to the re-use and mining of research data. According to standard scholarly practice, it is recommended to provide appropriate citation and attribution whenever technically possible.

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Aberrations in centrosome number and structure appear to have roles that go beyond multipolar spindle assembly and CIN in cancer cells. Cells with extra centrosomes have shown to cause altered chemokine and cytokine release (ECASP, extra centrosome-associated secretory pathway), ROS production, lysosomal dysfunction and disrupted autophagy (left yellow boxes). Furthermore, excessive CA can be observed in more invasive carcinomas and has been linked to motility, metastasis, cellular stiffness, and organelle re-positioning (right green boxes). Extra centrosomes can also activate NF-kB signaling and inflammation or BID-dependent apoptotic cell death in a PIDD1-dependent manner (lower blue boxes).