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. 2021 Jul 27;40(37):5613–5625. doi: 10.1038/s41388-021-01961-9

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© The Author(s) 2021

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. 6 — a Pearson correlation analysis of B-Myb and E2F2 in colorectal cancer samples (n = 177). b B-Myb upregulates E2F2 expression. Immunoblotting was performed to determine B-Myb and E2F2 expression in stable B-Myb overexpression and knockdown cells. c Schematic illustration of the wild-type and mutant E2F2-P1314 and B-Myb-P1064 luciferase (Luc) promoter reporter. The transcription start sites for E2F2 and B-Myb genes are indicated as +1. The E2F and Myb-binding sites are shown as boxes. The mutated E2F binding sites (EBS) and/or Myb-binding sites (MBS) are crossed. d Schematic illustration of the wild-type and mutant 3xE2F reporter and luciferase reporter assay. e, f Luciferase reporter assays. HCT116 cells were transiently transfected with the indicated plasmids, and 48 h after transfection, the luciferase activities were measured as described in “Materials and Methods” section. Data are expressed as fold change normalized to the activity of cells transfected with the empty pGL3-basic or pGL4.10 promoter-less vector alone (relative value, 1.0).