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Fig. 7 | Molecular Cancer

Fig. 7

From: CircMYH9 drives colorectal cancer growth by regulating serine metabolism and redox homeostasis in a p53-dependent manner

Fig. 7

CircMYH9 promoted colorectal tumorigenesis in p53 wild-type mice. A Scheme for the AOM/DSS-induced colon cancer model in p53WT and p53KO mice. One week before AOM injection, AAV9-circMYH9 and AAV-control were administered by enema. B Representative images of the visible tumors (arrows) in the p53KO, p53WT + Ctrl AAV and p53WT + AAV groups. C-E The tumour number, tumor incidence and tumor size in each group were analysed, data are shown as the mean ± SD (*, P < 0.05; **, P < 0.01). F The expression level of circMYH9 was detected by FISH in sections of tumours from each group. G The expression of p53, PHGDH and PSPH were detected by IHC in sections of tumours from each group. H Schematic representation showing that circMYH9 was amplified by amino acid starvation though the ROS-HIF1α pathway. circMYH9 destabilized the pre-mRNA of p53 by preventing hnRNPA2B1 binding to m6A sites on the 3' UTR of p53 pre-mRNA. Downregulation of p53 increased the expression of PHGDH, which maintained SG metabolism and redox homeostasis and promoted the growth and tumorigenesis of CRC

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