| Promotion of cancer cell proliferation mediated by the binding of AFP receptors (AFPR), |
| the activation of PI3K/AKT signal pathway, the stimulation of oncogene protein, and the |
| dysfunction of PTEN antioncogene protein [26–32]. |
| Promotion of tumor invasion and metastasis via upregulating expression of metastasis- |
| related proteins, such as keratin 19 (K19), epithelial cell adhesion molecule (EpCAM), |
| matrix metalloproteinase 2/9 (MMP2/9), and CXC chemokine receptor 4 (CXCR4) [26, 27, 33]. |
| Promotion of tumor angiogenesis by increasing expression of vascular endothelial growth |
| factor (VEGF), vascular endothelial growth factor receptor 2 (VEGFR-2), and |
| matrix metalloproteinases-2/9 (MMP2/9) [16, 26]. |
| Antitumor apoptosis by blocking the Fas/FasL, caspase-3, and PI3K/AKT signaling |
| pathways of tumor [13, 14, 16, 19, 27–29]. |
| Escaping from immune surveillance via triggering the Fas/FasL interaction between |
| tumor cells and lymphocytes; inhibiting the maturation and inducing apoptosis of DC |
| cells; reducing the secretion of the amount of IL-12 from DC cells, thus indirectly |
| inhibiting NK cell; promoting the change of CD4+ T and CD8+ T cell proportion; and |
| enhancing the quantity of Treg cells [20–25, 33–35]. |
