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. 2022 Sep 28;11:66. doi: 10.1186/s40164-022-00317-7

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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. 2 — The roles of p53 aggregation in tumor progression. (1) In normal cells, wild-type p53 is functional at the nucleolus and can regulate the cell cycle and preserve cell integrity. (2) In cells expressing an aggregation-prone mutant p53, mutant p53 can interact with homologs p63/p73 or Hsp70/90. p53 will be inactivated due to genomic or cancer cell-specific mutation events. (3) Aggregated p53 may interact with different proteins, such as p63/p73 and heat shock proteins. p53 aggregation might lead to the following three kinds of effects. (4) Loss-of function [LoF]: Losing wild-type activity, p53 is no longer active in the nucleolus. (5) Gain-of-function [GoF]: Acquire oncogenic activity without disrupting the activity of wild-type p53. (6) Dominant-negative [DN]: Inhibit the wild-type p53 protein via a dominant-negative effect and display oncogenic activity (GoF) or no other activity (LoF)