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. 2022 Aug 9;13:4680. doi: 10.1038/s41467-022-32472-0

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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. 5 — a, b The migration ability of 786-O cells after SNIP1 knockdown/overexpression as well as SNIP1 knockdown/overexpression together with DPF3a overexpression was measured using Transwell assay. Data were presented as mean values ± SD (n = 3 independent experiments). Statistical significance was estimated using a two-sided student t-test. Scale bar, 200 μm. c, d The metastatic ability of 786-O cells with SNIP1 knockdown and overexpression was measured using a mouse metastasis model. Tumor cells expressing luciferase were visualized with d-Luciferin as substrate using an in vivo imaging system. Total luminescence intensity was quantified and statistical significance was estimated using a two-sided student t-test. Data were presented as mean values ± SD (n = 4 animals). e The MA plot comparing the gene expression profile of 786-O cells with and without SNIP1 knockdown. The x-axis and y-axis represent Log2 (mean read counts) and Log2 (fold change), respectively. Red dots indicate upregulated genes, whereas blue dots indicate downregulated genes. The results represent two independent biological replicates. f Genome-wide co-occupancy of DPF3a and SNIP1. Average profiles and heatmaps of normalized read density of ChIP-seq for DPF3a and SNIP1 are presented. The results represent two independent biological replicates for each ChIP-seq experiment. g Genome browser view of ChIP-seq and RNA-seq normalized read counts at SNAI1, MMP2, COL1A1, and WNT7B loci. Co-binding regions of DPF3a and SNIP1 are marked with a red dashed box. h DPF3a ChIP experiments were performed in DPF3a-OE cells after SNIP1 knockdown and DPF3a enrichment at selected genes was quantified by qPCR. Data were presented as mean values ± SD (n = 3 independent experiments). Statistical significance was estimated using a two-sided student t-test (*p < 0.05). p_COL1A1 = 0.029, p_COL6A3 = 0.037, p_SNAI1 = 0.046, p_MMP2 = 0.016, p_MMP16 = 0.036, p_WNT7B = 0.023. i SNIP1 ChIP-qPCR was performed to compare its enrichment at selected genes in 786-O cells with and without DPF3a overexpression. Data were presented as mean values ± SD (n = 3 independent experiments). Source data are provided in the Source Data file.