Experimental study of allicin inhibiting the proliferation and invasion of human multiple myeloma cell

Objective To investigate the effect of allicin on the proliferation, apoptosis and invasion of human multiple myeloma (MM) cell line RPMI8226 in vitro, and to explore its mechanism. Methods The human MM cell line RPMI8226 cells were treated with different concentrations of allicin as 0, 5, 25, 125 μmol/L, wherein the control group was 0 μmol/L allicin treatment group. The proliferation of cells was calculated by cell counting kit-8 (CCK-8). The apoptosis and invasion ability of tumor cells were determined with flow cytometry and Transwell method respectively. The expressions of transforming growth factor-α (TGF-α), matrix metalloproteinase (MMP)-2, MMP-9 and tissue inhibitor of metalloproteinase-2 (TIMP-2) protein were detected by Western blotting. Results The proliferation rates of RPMI8226 cells in groups treated with 0, 5, 25 and 125 μmol/L allicin were 1.00%±0.02%, 0.98%±0.04%, 0.73%±0.22% and 0.44%±0.15% respectively, with a significant difference (F=329.2, P<0.001). The proliferation rates of RPMI8226 cells in the 25 and 125 μmol/L allicin treatment groups were significantly inhibited compared with control group (P<0.001; P<0.001); but there was no significant difference between 5 μmol/L treatment group and control group (P=0.395). The apoptosis rates of RPMI8226 cells treated with 0, 5, 25 and 125 μmol/L allicin were 3.05%±0.53%, 4.06%±0.29%, 12.17%±1.08% and 12.81%±1.78% respectively, with a significant difference (F=531.0, P<0.001). The apoptotic rates of RPMI8226 cells in the 25 and 125 μmol/L allicin treatment groups were significantly increased compared with control group (P=0.013; P=0.012); and there was no significant difference between 5 μmol/L treatment group and control group (P=0.211). The numbers of invasive cells in the 0, 5, 25 and 125 μmol/L allicin treatment groups were 112.5±1.9, 104.8±4.0, 76.9±2.6 and 52.5±3.7 respectively, with a significant difference (F=734.9, P<0.001). The abilities of cells invasiveness in 25 and 125 μmol/L allicin treatment groups were significantly decreased compared with control group (P<0.001; P<0.001), but 5 μmol/L allicin treatment group had no significant difference compared with the control group (P=0.160). Western blotting results showed that the expression levels of TGF-α, MMP-2, MMP-9 and TIMP-2 proteins were significantly different between groups treated with different concentrations of allicin (F=227.1, P<0.001; F=348.5, P<0.001; F=359.7, P<0.001; F=158.0, P<0.001). The protein expression levels of TGF-α, MMP-2 and MMP-9 were significantly decreased in the 25 and 125 μmol/L treatment groups compared with the control group (all P<0.001), and the expression of TIMP-2 protein was significantly increased compared with the control group (all P<0.001), but there were no significant diffe-rences between the 5 μmol/L treatment group and the control group (P=0.349; P=0.744; P=0.613; P=0.567). Conclusion Allicin can significantly inhibit cell proliferation, invasive ability and induce apoptosis of human MM cell line RPMI8226 in vitro, and the mechanism may be related to inhibiting the expressions of TGF-α, MMP-2, MMP-9 and promoting the expression of TIMP-2 at the same time. Key words: Multiple myeloma; Cell proliferation; Neoplasm invasiveness; Allicin