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. 2022 Feb 26;13(2):190. doi: 10.1038/s41419-022-04623-0

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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. 6 — The levels of N-cadherin (EMT signaling pathway), p-ERK (MEK/ERK pathway), and p-AKT (AKT/mTOR pathway) were evaluated using Western blotting, and the relative proliferation rate of 786-O (A) and A498 (B) cells transfected with LV-NC, miR-421 inhibitor, and miR-421 inhibitor+sh-CMTM4 was measured. Colony-formation assays (C, D), transwell assays (E, F), and wound-healing assays (G, H) were performed and quantitatively analyzed in 786-O cells transfected with LV-NC, miR-421 inhibitor, and miR-421 inhibitor plus sh-CMTM4. Data are presented as means ± SD. ***p < 0.001. The bar corresponds to 300 μm in the wound-healing assay.