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. 2020 Feb 11;11:834. doi: 10.1038/s41467-020-14581-w

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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. 1 — a HeLa cells were transfected with Myc-PIAS1 (PIAS1-OE) or Empty vector (NC-vector) for 48 h. PIAS1 overexpression efficiency was determined by western blotting. Actin was used as a loading control. b PIAS1 KO HeLa cells were generated by CRISPR/Cas9. PIAS1 KO was determined by western blotting. Actin was used as a loading control. c PIAS1 overexpression in HeLa cells significantly promotes cell growth, n = 3 biologically independent samples. d PIAS1 KO HeLa cells (PIAS1-sgRNA) showed impeded cell growth compared with the negative control cells (NC-sgRNA), n = 3 biologically independent samples. e PIAS1 overexpression increased cell migration as determined by a wound-healing assay. Scale bar: 200 μm, n = 5 biologically independent samples. f PIAS1 KO cells displayed decreased cell migration compared with the sgRNA-negative control cells, as determined by a wound-healing assay. Scale bar: 200 μm, n = 5 biologically independent samples. Data represent the mean ± SD, error bars represent SD, **p < 0.01, Student’s t-test. Source data are provided as a Source Data file.