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. 2020 Jul 8;11(7):515. doi: 10.1038/s41419-020-2713-8

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© The Author(s) 2020

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. 4 — a CCK-8 assays showed overexpressing CDCA3 reversed the proliferation-inhibition effect of si SNHG12 and knockdown CDCA3 reversed the proliferation-promoting effect of SNHG12 overexpression in ACHN and 786-O cells. b Migration and invasion ability attenuated by sh SNHG12 could be reversed by CDCA3 overexpression in ACHN and 786-O cells according to transwell assays (magnification: ×100). c Migration and invasion ability promoted by SNHG12 could be reversed by si CDCA3 according to transwell assays (magnification: ×100). d, e Cell cycle distribution was analysed by PI staining in ACHN and 786-O cells after co-transfection by sh SNHG12 and CDCA3 overexpression vector or SNHG12 overexpression vector and si CDCA3 for 48 h. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Error bars indicate mean ± SD.