Table 2.
Anti-metastatic action of 2S albumin component–Lunasin.
| Action | Mode of Action | Evidence |
|---|---|---|
| Inhibits cancer proliferation and induce apoptosis | Interaction with the αvβ3 integrin via the FAK/ERK/NF-κB signaling pathway; activation of caspase-3 and cleavage of PARP [73,74] | Inhibited the proliferation and the tumorsphere-forming capacity of colon cancer HCT-116 cells [75]. Increased the amount of colon cancer cells KM12L4 undergoing apoptosis twofold [76]. Reduced tumor growth in NSCLC and melanoma xenografts [72]. |
| Inhibits cancer cell invasion and migration | Interaction with cellular receptors (integrins and EGFR); disrupts the activity of key signaling proteins (MMP-2/-9) via the FAK/Akt/ERK and NF-κB signaling pathways [77] | Caused a reduction in the migration (scratch assay) of HCT-116 and KM12L4 colon cancer cells [74]. Inhibited the migration and invasion activity in MDA-MB-231 and MCF-7 breast cancer cell lines [77]. Inhibited the invasion of melanoma A375 and B16-F10 cells to matrigel [71]. |
| Reduces inflammation and oxidation | Reduction in the production of certain inflammatory markers (ROS, TNF-α and IL-6) [78,79] | Mouse macrophage cells (LPS-stimulated RAW 264.7) reduced the production of certain inflammatory markers (ROS, TNF-α and IL-6) [80]. |
| Reduces cancer cells colonization | Reduction in phosphorylation of the intracellular kinases FAK and AKT; reduction in histone acetylation of lysine residues in H3 and H4 histones [71] | Reduced pulmonary colonization after injection of highly metastatic B16-F10 melanoma cells [71,72]. Inhibited formation of liver metastasis in murine model [74]. |
| Arrest cell cycle | Arrests the cell cycle at the G2/M and G1/S phase; altered the expression of the G1 specific cyclin-dependent kinase complex components, increased levels of p27Kip1, reduced levels of phosphorylated Akt [76,81] | Inhibited cell cycle progression at the G1/S phase for NSCLC H661 cells [81]. Lunasin treatment of MDA-MB-231 breast cancer cells resulted in a notable increase in RB1 level, which lead to arrest of G1 phase [82] |