Fig. 4: Elevated HOX expression leads to an increase in cell cycle gene expression.
From: HOX genes promote cell proliferation and are potential therapeutic targets in adrenocortical tumours
a Heatmap of the top 50 differentially expressed genes identified from RNA-seq data of male ABC; Hoxb9 t/g adrenal tumours compared to male ABC adrenal tumours. b Comparison of differentially expressed genes in male and female ABC; Hoxb9 t/g adrenal tumours compared to ABC adrenal tumours. c Comparison of differentially expressed genes in male ABC; Hoxb9 t/g tumours compared in male ABC tumours to the genes differentially expressed genes in female ABC tumours compared to male ABC tumours. d STRING database network of differentially expressed genes in male ABC; Hoxb9 t/g tumours compared to male ABC tumours identifies angiotensin signalling. e qRT-PCR of Fos, Fosb and Junb in male ABC and ABC; Hoxb9 t/g tumours. The data represent mean ± SD from three biological repeats. f IHC of Fosb in 3-month-old male ABC; Hoxb9 t/g and ABC adrenal tumours. g GSEA of RNA-seq data from male ABC; Hoxb9 t/g and male ABC adrenal tumours. E2F targets normalised enrichment score (NES) = 1.57, FDR q = 0.069, G2M checkpoint NES = 1.70, FDR q = 0.043. h qRT-PCR of Cdk1, Ccnb1, Ccnb2, Ccne1 and Knstrn in female and male ABC and ABC; Hoxb9 t/g adrenal tumours. The data represent mean ± SD from three biological repeats. i Cell cycle genes upregulated in male ABC; Hoxb9 t/g tumours and female ABC tumours (compared to ABC males). Student’s t test, **P < 0.01, *P < 0.05. ABC indicates Ctnnb1 mutant tumours, ABC; Hoxb9 t/g indicates double-mutant tumours.
