PGK1 Antibody - #DF6722

Fig. 2 (A) Enrichment of glycolysis-related genes was significant in S100A9 positive BRCA cases (NES > 1, FDR q-value < 0.001). (B) S100A9 silencing impaired the expression of PGK1, LDHA, and ENO1 in both SK-BR-3 and BT474 cell lines. (C) IHC staining results of HER2+ BRCA tissues confirmed the upregulation of PGK1, LDHA, and ENO1 in S100A9 abundant cases (Scale bar = 100 μm, 200 μm, and 400 μm). (D) ECAR level significantly declined when S100A9 was absent from the SK-BR-3 and BT474 cell lines. (E) lactate production and glucose consumption level significantly declined when S100A9 was absent from the SK-BR-3 and BT474 cell lines. PGK1: Phosphoglycerate kinase 1. LDHA: Lactate dehydrogenase A. ENO1: Enolase α. ECAR: Extracellular acidification rate. S100A9: S100 calcium-binding protein A9. BRCA: Breast cancer. HER2: Human epidermal growth factor receptor 2. NES: Normalised enrichment score. FDR: False discovery rate. IHC:Immunohistochemical staining.

Fig. 3. IL13 secreted by YAP1-overexpressed GC cells stimulates resistance to 5-FU via inducing M2 subtype macrophage glycolysis reprogramming. A-C. RT-PCR was used to detect the mRNA expression of glycolysis enzymes, fatty acid and amino acid metabolism enzymes in THP1 after co-cultured with MKN-YAP1 or MKN45-Vetor. D. Protein level change of glycolysis enzymes in THP1 after co-cultured with MKN-YAP1, MKN45-Vetor, SGC7901-siYAP1 or SGC7901-NC. E. RT-PCR revealed the mRNA expression of glycolysis enzymes and M2 TAMs markers in THP1 after co-cultured with SGC7901-siYAP1 or SGC7901-NC. F-G. Relative lactate release from cells was determined by colorimetric analysis. Relative glucose uptake cells by Flow cytometry detection. All data presented are the mean ± SD (*p < 0.05, **p < 0.01) of triplicate determination from three independent experiments.