Fig. 5

FMD inhibits pro-tumor migration of TAMs by mTOR phosphorylation. A Immune cell infiltration is analyzed using data from GEO (dataset GSE50712, Control vs. EVE-treated breast tumor bearing mice). B Glucose consumption of TAMs under hypoxia with EVE (100 nM), 2ME2 (10 µM), or 2-DG (10 mM) for 72 h is determined by glucose assay. C Lactate acid in the medium supernatant of TAMs under hypoxia with EVE (100 nM), 2ME2 (10 µM), or 2-DG (10 mM) is detected by lactate acid assay after 72 h. D The cell viabilities of TAMs under hypoxia with EVE (100 nM), 2ME2 (10 µM), or 2-DG (10 mM) for 72 h are detected by CCK-8 assay. E The mRNA expression of Arg1, CD163, CD206, and IL-10 in TAMs treated for 72 h with low (EVE(L), 50 nM) or high doses of EVE (EVE(H), 100 nM), are measured by RT-PCR. F Migration of MDA-MB-231 cells after co-incubation with TAMs is determined in Transwell assays (magnification, ×10). Data are presented as the means ± S.E.M. from three separate experiments. *P < 0.05, **P < 0.01, vs. respective control group