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. 2022 Oct 8;13(10):858. doi: 10.1038/s41419-022-05307-5

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© The Author(s) 2022

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — All three PLEKHH2-siRNAs down-regulated endogenous PLEKHH2 expression. A Cell lines transfected with PLEKHH2-siRNA plasmid showed decreased PLEKHH2 expression. Clone formation assay (B) and CCK-8 assay (C) showed that PLEKHH2-siRNA treatment led to a decrease in cell proliferation. The Scratch wound assay (D), Transwell migration assay (E), Matrigel Transwell assay (F), and 3D invasion experiment (G) showed that PLEKHH2 knockdown inhibited the biological functions of lung cancer cells, including migration and invasion. Western blotting showed that downregulation of PLEKHH2 decreased the expression of proliferation- and invasion-related proteins, including MMP2, MMP9, CDK4, CDK6, CyclinD1, CyclinE, RhoA, RhoC, and Cdc42 (H). The other two siRNAs showed similar changes, as shown in Supplementary Fig. 1 and Supplementary Fig. 2. P < 0.05 indicates statistical significance, *P < 0.05, **P < 0.01, ***P < 0.001.