Objective The aim of this study was to investigate the expression of intercellular adhesion molecule 1 (ICAM1) in human hepatocellular carcinoma (HCC) and to analyze the correlation between its expression level and the metastatic ability of liver cancer stem cells.

Methods Human liver cancer stem cell lines LCSC1, LCSC2, LCSC3, and LCSC4 with different metastatic potentials, as well as liver cancer cell lines HUH-7 and Hep3B were cultured in vitro. Real-time fluorescence quantitative polymerase chain reaction (qPCR) and Western blot were used to detect the expression level of ICAM1 in each cell line. Transwell migration assay and wound healing assay were used to evaluate the migration ability of LCSC2, LCSC3, HUH-7, and Hep3B liver cancer cells. After knocking down ICAM1, the migration ability of LCSC2, LCSC3, HUH-7, and Hep3B cells was evaluated by Transwell migration assay. We established a liver metastasis model mouse and detected the expression level of ICAM1 in the metastatic lesions and primary lesions in mice by Western blot. After the treatment with OSMI-1 drug, the protein expression levels of ICAM1 in LCSC3 and LCSC1 cells were detected by Western blot, and the migration ability change of LCSC3 was verified by wound healing assay.

Results In liver cancer stem cells, both mRNA and protein expression levels of ICAM1 in cells with high migration ability were significantly higher than those in cells with low migration ability, and the difference was statistically significant (P<0.05). When ICAM1 was knocked down, the migration ability of LCSC2, LCSC3, HUH-7 and Hep3B cells was significantly reduced compared with the control group. In the mouse liver metastasis model, the expression of ICAM1 in the metastatic lesion was higher than that in the primary lesion. In addition, after OSMI-1 drug treatment, the protein expressions of ICAM1 in LCSC3, LCSC1 cells were reduced compared with the control group, and the scratch test results verified significant reduction of the migration ability of liver cancer stem cells after drug treatment.

Conclusion The high expression of ICAM1 in human liver cancer was closely related to the metastasis process of cancer cells. The knockdown of ICAM1 could effectively inhibit the metastatic ability of LCSC2, LCSC3, HUH-7 and Hep3B cells. These findings provide important scientific basis and new ideas for finding potential therapeutic targets against liver cancer stem cell metastasis.