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. 2021 Mar 5;12(3):250. doi: 10.1038/s41419-021-03539-5

Fig. 3. Transcriptional repression of p62 via DNA methylation increases in vitro tumorigenicity of HN9-R clones.

Fig. 3

A Western blot analysis of p62, NCoR1, HDAC1, DNMT1, and histone modification proteins in HN9 cells. The numbers below the gel lines represent the protein level relative to HN9-P cells, which was determined form the band intensity and normalized by β-actin. B Variation in H3 modifications on the p62 promoter in HN9 cells. The ChIP assay shows transcriptionally active histone markers (Ac-H3 and H3K4me3) enriched on the promoter in HN9-S and an inactive marker (H3K27me3) detected on the promoter in HN9-R. The results obtained from three independent biological replicates were represented as percentage of input (% input). C, D Proliferative capacity (C) and colony formation (D) of DNMT1-depleted HN9 cells. Results are presented as means ± standard error of the mean (SEM). *p < 0.05; **p < 0.01.