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. 2022 Jan 14;8:26. doi: 10.1038/s41420-021-00791-8

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© The Author(s) 2022

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — Ionizing radiation induces the nuclear translocation of Rac1, the latter then binds with p53 and prolongs the residence time of p53 in the nucleus, thereby promoting the transcription of Trp53inp1 which mediates p53-dependent apoptosis. Inhibition of Rac1 with NSC23766 could reduce the nuclear translocation of Rac1 induced by irradiation, thereby fasting the release of p53 from the nucleus, at last reducing the apoptosis. In addition, Rac1 inhibition could also significantly reduce ROS generation, but have no effect on the proliferation of MLE. In contrast, due to the overexpression and mutation of Rac1, inhibition of Rac1 does not reduce the apoptosis of tumor cells after radiation but can inhibit the proliferation ability of tumor cells significantly.