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. 2021 Oct 9;19:417. doi: 10.1186/s12967-021-03087-8

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© The Author(s) 2021

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — CENPA promoted the proliferation, migration and invasion of ccRCC cells. CENPA A, B mRNA (n = 3 per group) and C protein levels were verified by qRT-PCR in A498 and Caki-1 cells with transient CENPA knockdown or overexpression. D–F Cell viability of A498 and Caki-1 cells after depleting or overexpressing CENPA was calculated using CCK-8 assays for four days (n = 6 per group). H The cell migration and invasion ability of transfected A498 and Caki-1 cells were evaluated using transwell assays (Magnification: 200×, n = 3 per group). *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. Error bars indicate mean ± SD