Skip to main content
. 2017 Apr 7;8:14922. doi: 10.1038/ncomms14922

Figure 3. Loss of histone H3 lysine 27 trimethylation accompanies SCC transition.

Figure 3

(a) Western blotting analysis performed on whole-cell extracts from tumours of the indicated genotypes and histologies. Histone H3 lysine 27 tri-methylation (H3K27me3) is markedly lower in SCC lesions; total histone H3 is the loading control. (b) Western blotting analysis performed on whole-cell extracts from tumours of the indicated genotypes and histologies. p63 and LKB1 confirm the histologies and genotypes of the lysates, and while EZH2 in more highly expressed in SCC tumours, the essential PRC2 subunit EED is absent in the SCC lesions. β-Actin is the loading control. (c) Immunohistochemisty for H3K27me3 on a panel of mouse lung tumours of the indicated histologies from KRAS/Lkb1, Pten/Lkb1/p53, and Pten/Lkb1 mice, scale bar, 50 μm. (d) Quantification of nuclear staining by dot analysis with Nikon software; data are mean±s.e.m. measured on serially stained sections, n=6–10. (e) Immunohistochemisty for H3K27me3 on a panel of human mixed adenocarcionomas, pure ADC and pure SCCs. Scale bar, 50 μm. (f) Quantification of nuclear staining, for H3K27me3 n=6 ADSCC, 14 ADC, 9 SCC, for EZH2 n=6 ADSCC, 7 ADC, 5 SCC, data are mean±s.e.m. measured on serially stained sections. P values represent 2 tailed t-test. See also Supplementary Fig. 3a–c.