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. 2021 Feb 2;11:621757. doi: 10.3389/fimmu.2020.621757

Figure 2.

Figure 2

Upregulated V-ATPase activity conferred resistance to macrophage-mediated PrCR. (A) Pharmacological inhibition of V-ATPase with concanamycin A (10 nM) diminished extracellular acidification of P10 cells. **P < 0.01 (one-way ANOVA test). (B) A phagocytosis assay with BMDMs showing that concanamycin A treatment restored the vulnerability of P10 cells to macrophage-mediated PrCR. Each group was compared with the WT group. **P < 0.01 (one-way ANOVA test). (C) Significant up-regulation of V-ATPase subunit coding genes in breast cancer (n=1,102) tissues as compared to the adjacent normal tissues, based on TCGA datasets (In total 10 ATPase H+ Transporting V0 subunit protein coding genes, 13 ATPase H+ Transporting V1 subunit protein coding genes and 3 ATPase H+ Transporting accessory protein coding genes were included into the analysis). *P < 0.05 (t test). (D) A phagocytosis assay with BMDMs showing that knocking-down the expression of the individual subunit of V-ATPase with CRISPR increased the susceptibility of SW620 cells to PrCR. Each group was compared with the CtrlKD group. **P < 0.01 (one-way ANOVA test).