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. 2020 Sep 7;20:439. doi: 10.1186/s12935-020-01527-x

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© The Author(s) 2020

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 — Peak visualization of 5 ChIP-Seq datasets of KLF5 on SNHG12 and its expression pattern. a The signals of the 5 ChIP-Seq datasets of KLF5 are shown. The picture shows that the promoter of SNHG12 has a high KLF5 binding signal in 5 samples. b The top 10 enriched GO BP terms of SNHG12 co-expressed partners in CRC. c The top 10 enriched KEGG pathways of SNHG12 co-expressed partners in CRC. d The expression level of SNHG12 in CRC tissues was significantly higher than that in adjacent normal tissues. e SNHG12 expression levels were up-regulated in CRC cell lines (HCT116, HT29, SW620, and COLO-205) compared with the normal colon epithelial cell line (NCM460)