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Tunicamycin ( TM ) is an  N ‐linked glycosylation ( NLG ) inhibitor with strong antitumor activity, the exact underlying molecular mechanism of which remains to be elucidated. In our previous studies, we found that  TM  reversed drug resistance and improved the efficacy of combination treatments for hepatocellular carcinomas ( HCC ). Here, we investigated the effects of  TM  on  HCC  cell proliferation and migration as well as the mechanism of those effects. Our results showed that  TM  inhibited cell proliferation and migration as well as induced apoptosis of hepatocellular carcinoma cells.  TM  inhibited proliferation of  HCC  cells by inducing cell apoptosis and cell cycle arrest at the G2/M phase. Meanwhile,  TM  inhibited migration of  HCC  cells by suppressing  CD 44s‐mediated epithelial‐mesenchymal transition ( EMT ).  TM  inhibited migration and invasion of  HCC  cells by decreasing  CD 44 expression and altering its glycosylation. In addition,  CD 44s is involved in promoting  EMT  and is associated with a poor prognosis in  HCC  patients. Overexpression of  CD 44s promoted tumor migration and activated phosphorylation of  ERK 1/2 in  HCC  cells, whereas  TM  inhibited  CD 44s overexpression‐associated cell migration. The ability of  TM  to inhibit cell migration and invasion was enhanced or reversed in  CD 44s knockdown cells and cells overexpressing  CD 44s, respectively. The  MEK / ERK  inhibitor U0126 and  TM  inhibited hyaluronic acid‐induced cell migration in  HCC  cells. Furthermore,  TM  inhibited exogenous transforming growth factor beta ( TGF ‐β)‐mediated  EMT  by an  ERK 1/2‐dependent mechanism and restored the  TGF ‐β‐mediated loss of E‐cadherin. In summary, our study provides evidence that  TM  inhibits proliferation and migration of  HCC  cells through inhibition of  CD 44s and the  ERK 1/2 signaling pathway.

Tunicamycin inhibits cell proliferation and migration in hepatocellular carcinoma through suppression of CD 44s and the ERK 1/2 pathway