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. 2024 Dec 28;14:31327. doi: 10.1038/s41598-024-82793-x

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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. 5 — Silencing IQGAP3 and GLI reduced the migration, invasion and stemness potential of lung cancer. (A-B) Representative images and quantified data from wound healing assays conducted in H1299 cells after down-regulating IQGAP3 and GLI1. Scale bar = 200 μm. (C-D) Representative images and quantified data illustrating Transwell migratory assays performed in H1299 and A549 cells after silencing IQGAP3 and GLI1. Scale bar = 50 μm. (E-F) Evaluation of invasion ability in H1299 and A549 cells using Transwell invasive assays after IQGAP3 and GLI1 down-regulation. Scale bar = 50 μm. (G-H) Sphere formation ability of lung cancer cells assessed through sphere formation assays after IQGAP3 and GLI1 silencing. Scale bar = 100 μm. Data represent mean ± SD from experiments conducted in triplicate. **P < 0.01, ***P < 0.001, ns not significant.

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