Research Paper Volume 16, Issue 12 pp 10512—10538

The crosstalk role of CDKN2A between tumor progression and cuproptosis resistance in colorectal cancer

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Figure 4. The impact of CDKN2A on energy metabolism, copper metabolism, and copper ion transportation. (A) UMAP dimension reduction plots of colorectal cancer epithelium cells showing the expression level of CDKN2A, with color depth representing the level of CDKN2A expression and gray indicating undetected CDKN2A expression. (B) Reactome metabolic pathways for different CDKN2A expression levels in tumor epithelium cells. (C) KEGG metabolic pathways for different CDKN2A expression levels in tumor epithelium cells. (D) Knockdown of CDKN2A leads to a decrease in the mRNA expression levels of phosphofructokinase-1 genes (PFKM, PFKL) in CRC cell lines. (E) Comparison of copper metabolism scores among different CDKN2A expression groups in tumor epithelial cells. ***P < 0.001, Wilcoxon test. (F) A scatter plot was generated to illustrate the correlation between CDKN2A expression and copper metabolism in the TCGA cohort. (G) qRT-PCR was utilized to examine the impact of CDKN2A knockdown on the mRNA transcriptional levels of copper transporters (SLC31A1, SLC31A2, ATP7B) in CRC cell lines. (H) Knocking out CDKN2A increases the intracellular copper ion concentration. ns represents no significance; *P < 0.05, **P < 0.01, ***P < 0.0001.