Abstract
Migration-inducing gene 7 (MIG7) is highly expressed and is implicated in multiple malignant tumors with vasculogenic mimicry (VM) which renders possible routes without the endothelium for invasion and metastasis. However, there are few reports in the literature describing the relationship between MIG7 expression and VM formation in hepatocellular carcinoma (HCC). In the present study, we found a significantly positive correlation between MIG7 expression and VM in 40 HCC specimens. Three-dimensional (3D) culture showed that VM formation in the HCC cell line MHCC-97H with high metastatic potential was enhanced to a greater extent than that of MHCC-97L and Huh-7 with low and non-metastatic potential. There was no VM formation in human normal hepatocyte line L-02. Moreover, MIG7 expression was higher in MHCC-97H than in MHCC-97L and Huh-7 cells and non-detectable in L-02 cells. MIG7 knockdown in MHCC-97H cells reduced VM formation, and weakened the invasive properties accompanying the enhanced cellular adhesion. Notably, there was no significant effect of endostatin (ES), a broad-spectrum angiogenesis inhibitor applied to clinical treatment, on both MIG7 expression and VM formation. Thus, the present study presents a causal link between MIG7 expression and VM formation in HCC, suggesting a potential treatment target for invasion and metastasis.
Highlights
Hepatocellular carcinoma (HCC) is one of the most common malignancies, and is the second leading cause of cancerrelated death worldwide [1]
The results showed that there was a positive correlation between Migration-inducing gene 7 (MIG7) expression and vasculogenic mimicry (VM) formation. there was no MIG7 expression and VM formation in normal liver tissues
These results showed that there was a positive correlation between VM formation and the metastatic potential of the HCC cell lines
Summary
Hepatocellular carcinoma (HCC) is one of the most common malignancies, and is the second leading cause of cancerrelated death worldwide [1]. The metastasis and recurrence of HCC has become one of the major obstacles to the therapeutic treatment of HCC. Blood vessels are considered as a main route of HCC metastasis, vasculogenic mimicry (VM) has been certified to be a potential bypass for metastasis. In VM, tumor cells arrange in lines to form vessel-like structure effectively mimicking a true vascular endothelium, which provide tumors with blood perfusion and promote tumor metastasis [4,5]. VM has been reported in HCC [6] and other types of tumors including ovarian cancer [7], melanoma [8], osteosarcoma [9] and prostatic cancer [10]
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