Abstract
The intestinal metabolite of ginseng saponin, compound K (CK), has various chemopreventive
and chemotherapeutic activities, including anti-tumor activity. However, the functional
mechanisms through which CK attenuates metastatic growth in hepatocellular carcinoma
(HCC) remain unclear. Here, using multiple in vitro and in vivo models, we reported that CK strongly attenuated colony formation, adhesion, and invasion
of HCC cells in vitro and dramatically inhibited spontaneous HCC metastatic growth in vivo . At the molecular level, immunofluorescence and Western blotting analysis confirmed
that inhibition of metastatic growth of HCC induced by CK treatment caused a time-dependent
decrease in nuclear NF-κ B p65 and a concomitant increase in cytosolic NF-κ B p65, indicating that CK suppressed the activation of the NF-κ B pathway. Meanwhile, our study showed that the inhibition of matrix metalloproteinase2/9
(MMP2/9) expression caused by CK treatment was associated with NF-κ B p65 nuclear export. Taken together, our results not only revealed that NF-κ B p65 nuclear export and the reduction of MMP2/9 expression were associated with the
metastatic inhibition induced by CK, but also suggested that CK may become a potential
cytotoxic drug in the prevention and treatment of HCC.
Key words
compound K - ginsenoside - hepatocellular carcinoma - matrix metalloproteinase‐2/9
- NF‐κ B p65
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gangsongsd@xmu.edu.cn
