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. 2024 Feb 6;14:3014. doi: 10.1038/s41598-024-53422-4

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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/.

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TRIM59 promoted LSCC cells metastasis through PI3K-AKT pathway. (A) The qRT-PCR assay showed that TRIM59 was upregulated in 50 LSCC tissues compared with adjacent noncancerous tissues. (B) The qRT-PCR assay showed the knockdown efficiency of transient transfection with pGenesil-1 (NC) and shRNA of TRIM59 in LSCC cells. (C) The WB analysis demonstrated the reduction in phosphorylation level of PI3K and AKT with TRIM59 knockdown in LSCC cells. The original blots were presented in Supplementary Fig. 1G. Cell biological function assays, (D) Colony formation assay showed TRIM59 knockdown inhibited the proliferation ability of TU177 and AMC-HN-8 cells. (E) MTS assay showed TRIM59 knockdown restrained the proliferation ability of TU177 and AMC-HN-8 cells. (F) Transwell assays showed TRIM59 knockdown attenuated the migration and invasion ability of TU177 and AMC-HN-8 cells. Data represents mean ± S.D. from three independent experiments. ns, not significant; *p < 0.05; **p < 0.01; ***p < 0.001.