Ginsenoside F4 inhibits colorectal cancer progression by boosting dendritic cell maturation and remodeling the tumor microenvironment

Figure 4 F4 promoted the maturation of dendritic cells via activation of phosphoinositide 3-kinase/protein kinase B and nuclear factor kappa-B pathways. A and B: F4 promoted the maturation of dendritic cells (DCs) and the production of inflammatory cytokines, which could be reversed by sphingosine-1-phosphate 1 (S1PR1) inhibitor fingolimod hydrochloride (FTY720); C and D: F4-stimulated DCs enhanced cytotoxic T lymphocyte response against the proliferation of CT26 cells, which could be depleted by S1PR1 inhibitor FTY720; E: F4 upregulated the expressions of phosphorylated phosphatidylinositol 3-kinase, phosphorylated protein kinase B and nuclear factor kappa-B phosphorylated-p65 in DCs, which could be reversed by S1PR1 inhibitor FTY720. All data were shown as mean ± SD (n = 5). ^aP < 0.05. ¹P vs control group (0 μg/mL F4 + 0 μM fingolimod hydrochloride). ²P vs 50 μg/mL F4-treated group. CD: Cluster of differentiation; IL: Interleukin; FTY720: Fingolimod hydrochloride; mRNA: Message RNA; PI3K: Phosphatidylinositol 3-kinase; p-PI3K: Phosphorylated phosphatidylinositol 3-kinase; AKT: Protein kinase B; p-AKT: Phosphorylated protein kinase B; NF-κB: Nuclear factor kappa-B.