Fig. 6 | Scientific Reports

Fig. 6

From: Single-cell multi-omics uncovers CPS1 as a breast cancer immune evasion therapeutic target

Fig. 6

CPS1 expression and functional validation in breast cancer. (A) CPS1 mRNA expression was higher in TCGA-BRCA tumor tissues than in normal tissues (p < 0.01). (B) Overall survival was worse in TCGA-BRCA patients with high CPS1 expression (p < 0.0001). (C) The AUC of CPS1 expression predicting 1-, 3-, and 5-year survival were 0.70, 0.61, and 0.55, respectively. (D) Single-cell analysis showed (GSE176078) that CPS1 expression was significantly higher in some cell types (e.g., oligodendrocytes and fibroblasts) than in others (e.g., B lymphocytes and endothelial cells). (E) CPS1 expression is higher in malignant epithelial cells than in non-malignant cells. (F-G) qpcr validation of the knockdown efficiency of cps1 in bt549 (F) and e0771 (G) cells showed that the cps1 gene was successfully knocked down in bt549 and e0771 cell lines. (H–J) Knockdown of CPS1 reduced colony formation in BT549 and E0771 cells. (K–M) Proliferation of BT549 and E0771 cells was diminished after cps1 knockdown. (M) ECAR decreased after CPS1 knockdown, with significant differences in sh#2 (p < 0.01, *** p < 0.001). (N, O) Glycolytic activity was significantly reduced in the CPS1 knockdown group. (P) Real-time ECAR in BT549 cells showed reduced glycolysis in the knockdown group. (Q) Western blot showed reduced expression of Pan-Kla and h3k9la in the knockout group, suggesting that cps1 is involved in epigenetic and transcriptional regulation of breast cancer cells by regulating histone h3 lactonylation modification.

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