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. 2023 Aug 18;13:153. doi: 10.1186/s13578-023-01094-4

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© The Author(s) 2023

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/. 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. 6 — The NUDC/cofilin1-dependent cytoskeleton is involved in the PUS10-induced migration suppression of RCC. A KEGG enrichment analysis of the genes possessing a negative correlation with PUS10 in KIRC. B, C The efficiency of NUDC silencing was demonstrated at the mRNA and protein levels. D Transwell assays revealed that NUDC depletion abrogated the promoted migration caused by PUS10 knockdown in Caki-1 and 786-O cells. Migrating cells in three replicate experiments were counted and are presented as the mean ± SD in the histogram. E Wound healing assays showed that NUDC depletion reversed the enhanced wound healing rate induced by PUS10 knockdown in Caki-1 and 786-O cells. Three replicate experiments were conducted, and the results are presented as the mean ± SD in the histogram. F Representative images of immunostaining using anti-cofilin1 antibody and phalloidin are shown, showing the impact of PUS10 on the cofilin1-dependent cytoskeleton. G Western blot assays showed that the increased expression of Coflin1 induced by PUS10 knockdown was rescued by NUDC depletion in Caki-1 and 786-O cells. *P < 0.05, **P < 0.01, ***P < 0.001; ns not significant