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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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CircMMP9 enhanced LSCC progression via TRIM59. (A) The WB analysis showed that the increased phosphorylation level of PI3K and AKT caused by circMMP9 overexpression could be rescued by TRIM59 knocking down. The original blots were presented in Supplementary Fig. 1H. Cell biological function rescued assays (B) Colony formation assay showed that TRIM59 knockdown weakened the proliferation ability of TU177 and AMC-HN-8 cells caused by circMMP9 overexpression. (C) MTS assay showed TRIM59 knockdown reduced the proliferation ability of TU177 and AMC-HN-8 cells induced by circMMP9 overexpression (black stars represent the comparison between NC + NC and circMMP9 + NC; blue stars represent the comparison between circMMP9 + NC and circMMP9 + sh-TRIM59). (D)Transwell assays showed TRIM59 knockdown weakened the migration and invasion ability of TU177 and AMC-HN-8 cells contributed by circMMP9 overexpression. (E) The mechanism diagram of circMMP9 promoted LSCC progression. Data represents mean ± S.D. from three independent experiments. ns, not significant; *p < 0.05; **p < 0.01; ***p < 0.001.