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. 2020 Nov 26;8:559486. doi: 10.3389/fcell.2020.559486

FIGURE 6.

FIGURE 6

S100A10 promotes tumor growth in vivo. (A–C) S100A10 overexpression promoted tumor growth in vivo. This effect could be rescued by rapamycin. (D) Expression of downstream effector genes of S100A10 was evaluated in mouse xenograft tumors. The expression levels of p-Src, p-ANXA2, p-mTOR, GLUT1, LDHA, and PFKFB3 were significantly higher in the OE-S100A10 group compared with negative control group. (E) A schematic model of the role and mechanism of S100A10 in GC glycolysis. Ectopic S100A10 expression increases Src kinase activity, resulting in the phosphorylation of S100A10 binding protein, ANXA2, which in turn activates the AKT/mTOR signaling pathway and further upregulates the activity of key glycolytic enzymes to enhance aerobic glycolysis and malignant growth and suppress cell apoptosis in GC. OXPHOS, oxidative phosphorylation; TCA cycle, tricarboxylic acid cycle; and ATP, adenosine triphosphate.