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. 2025 Jan 6;15:954. doi: 10.1038/s41598-024-82109-z

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 4 — Knockdown of SLCO4A1-AS1 affects glioma cell proliferation. (A) Based on qRT‒PCR analysis, the SLCO4A1-AS1 expression levels in LN229, A172, U118, GBM#P3, GBM#BG5 and GBM#BG7 cells were higher than those in NHA (n = 3). (B) Knockdown efficiency of siRNAs in LN229, A172, U118, GBM#P3 and GBM#BG5 cells (n = 3). (C) CCK-8 assay results showing that knockdown of SLCO4A1-AS1 inhibits the proliferation of LN229, A172, U118 and GBM#P3 cells (n = 3). (D) Transfection with siRNAs targeting SLCO4A1-AS1 reduces the colony-forming ability of LN229, A172 and U118 cells (n = 3). (E) Proliferative activity of glioma cells after knockdown of SLCO4A1-AS1 analyzed by EdU assay (n = 3). Scale bar = 50 μm. Data are presented as the mean ± SD. NS, not statistically significant; * P < 0.05; ** P < 0.01; *** P < 0.001. 2-way ANOVA (C) and 1-way ANOVA (A, B, D and E) were used for data analysis.