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. 2020 Jun 8;10:76. doi: 10.1186/s13578-020-00440-0

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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. 5 — KLF13 reduces cholesterol biosynthesis and transcriptionally represses HMGCS1. a Cholesterol content was detected in shCtrl, shKLF13#1 and shKLF13#2 HCT116 and HT-29 cells. *p < 0.05. b Cholesterol content was detected in Ctrl and KLF13 overexpressed HCT116 and HT-29 cells. *p < 0.05. c shCtrl and shKLF13#1 HCT116 or HT-29 cells were subjected to RT-qPCR and Western blot analysis of HMGCS. **p < 0.01. d Ctrl and KLF13 overexpressed HCT116 or HT-29 cells were subjected to RT-qPCR and Western blot analysis of HMGCS. **p < 0.01. e Luciferase activity of HMGCS1 promoter was measured in siCtrl, siKLF13, Ctrl and KLF13 overexpressed HCT116 and HT-29 cells. **p < 0.01. f ChIP-qPCR assay was performed in KLF13 knockdown HCT116 and HT-29 cells to determine KLF13 binding to HMGCS1 promoter. **p < 0.01