Fig. 1
From: Inhibition of Bcl6b promotes gastric cancer by amplifying inflammation in mice
Bcl6b was downregulated by promoter methylation along with activated inflammation throughout the progression of BaP-induced gastric carcinogenesis in mice. (a) Representative images showing H&E staining of stomachs (Scale bar, 100 μm) and immunostaining of Ki-67 and Bcl6b expression in mouse gastric samples (Scale bar, 50 μm) throughout the progression of BaP-induced carcinogenesis. (b) qRT-PCR revealed Bcl6b mRNA levels in mouse gastric samples during the progression of BaP-induced carcinogenesis. (c) A typical CpG island spans the promoter region of mouse Bcl6b. Each vertical bar represents a single CpG site. The transcription start site (TSS) is indicated by a curved arrow. Bisulphite genomic sequencing (BGS) analysis revealed the methylation status of Bcl6b in mouse gastric samples during the progression of BaP-induced carcinogenesis. Filled circles: methylated CpG sites; open circles: unmethylated CpG sites. (d, e) qRT-PCR revealed the TNF-α, IL-1β and IL-8 mRNA levels in mouse gastric samples (D) and ELISA revealed the serum protein levels of TNF-α and IL-1β (e) during the progression of BaP-induced gastric cancer in mice. Data are presented as the mean ± SD; n = 5 per group. *P < 0.05; **P < 0.01; ***P < 0.001; unpaired two-tailed Student’s t tests