Figure 7.

AHNAK attenuates cellular global p53 response, and its loss makes cancer cells more sensitive to cancer treatment

(A and B) Gene set enrichment analysis for co-expression of AHNAK with genes of the ontology “transcriptional regulation by TP53” in 28 different cancer transcriptome datasets and differentiation by TP53 mutation in stomach cancer.

(C) Comparison of correlation coefficients (Spearman’s R) between co-expressed genes with AHNAK versus co-expression with TP53BP1, differentiated by TP53 mutation status in stomach cancer. Density lines indicate the density of genes in the two-dimensional (2D) space, where “other genes” (green) are all genes not assigned to the ontology of “transcriptional regulation by p53” (orange).

(D) Differentiation of AHNAK expression in stomach cancer by TP53 status (i.e., mutation and/or deletion). The p value is derived from Wilcoxon testing.

(E) WT and two independent AHNAK^−/− U2OS cell lines were treated with fixed concentration of Nutlin and increasing concentration of etoposide.

(F) BJ fibroblast transfected with AHNAK siRNA or control and treated with fixed concentration of Nutlin-3 and increasing concentration of etoposide.

(G) Coefficient of drug interaction (CDI) analysis (see STAR Methods) of Nutlin and etoposide as in (E) and (F).