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. 2019 Jun 24;10(7):499. doi: 10.1038/s41419-019-1694-y

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© The Author(s) 2019

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. 7 — a DNA-pull down assay revealed the interaction between FOXP1 transcription suppressor and CLRN1-AS1. b The expression level of FOXP1 was in tumor samples and normal samples. c Correlation analysis of expression correlation between FOXP1 and CLRN1-AS1 in tumor samples. d qRT-PCR analysis of CLRN1-AS1 expression in PPA cells transfected with sh-FOXP1 or pcDNA-FOXP1. e, f DNA motif of FOXP1 and predicted five binding sites of FOXP1 in CLRN1-AS1 promoter. g ChIP assay revealed that P2 was responsible for the affinity of FOXP1 to CLRN1-AS1 promoter. h The effect of FOXP1 overexpression or knockdown on luciferase activity of vector containing CLRN1-AS1 promoter was abolished when site 5 was mutated. ^**P < 0.01, ^***P < 0.001 versus control group, indicated data are statistically significant