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. 2019 Apr 17;9:6212. doi: 10.1038/s41598-019-42707-8

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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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Lgr5⁺ specific-deletion of PKM2 accelerates development of inflammation-induced CRC. (a) Treatment scheme for AOM/DSS colon cancer model. PKM2^f/fxLgr5^CreERT2 mice were injected with vehicle (Veh) or tamoxifen (Tx) following induction of colon cancer by treatment of AOM and DSS. (b) Weight loss (n = 32) and (c) representative images of colons from AOM/DSS-treated PKM2^ΔLgr5 mice. (d) Tumor load (n = 17 for Veh, n = 18 for Tx) and tumor size (n = 15 for Veh, n = 17 for Tx) in AOM/DSS-treated mice. (e) Colon histology of AOM/DSS-treated mice. Arrowheads indicate colon polyps. Representative images of low- and high-grade dysplasia and adenocarcinoma. Scale bar = 100 μm. H&E stained sections were scored for severity and area of dysplasia (n = 4 for Veh, n = 6 for Tx). All data are mean ± s.e.m. Statistical analyses were done by Student’s t-test or two-way ANOVA with Bonferroni post-hoc test. *p < 0.05, **p < 0.01.