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Interferon-stimulated gene 15 (ISG15) serves a crucial role in hepatocellular carcinoma (HCC) progression. The present study explored the effect of ISG15 knockdown on the sensitivity of HCC cells to norcantharidin. The expression of ISG15 in HCC tissues and cell lines was assessed by reverse transcription-quantitative polymerase chain reaction and immunohistochemistry. Pearson's χ 2 test was conducted to analyze the correlation between the clinicopathological features and ISG15 expression of patients with HCC. In addition, HCC cells were transfected with small interfering RNA against ISG15, ISG15 overexpression plasmid or respective negative controls. Cell proliferation, clonogenic ability and apoptosis were examined by Cell Counting Kit-8, colony formation and Annexin V/propidium iodide staining assays, respectively. Protein expression was assessed by western blot analysis. The results revealed that ISG15 was overexpressed in HCC tissues, and that ISG15 expression was positively correlated with HCC differentiation and metastasis. Downregulation of ISG15 increased the sensitivity of HCC cells to norcantharidin, and norcantharidin treatment reversed the tumor-promoting effects of ISG15 overexpression exerted in HCC cells. Furthermore, the expression levels of apoptosis-associated proteins were regulated by ISG15 and norcantharidin. Taken together, the observed increase in the sensitivity of HCC cells to norcantharidin was facilitated by ISG15 knockdown and may provide novel insights for HCC therapy.

Knockdown of interferon‑stimulated gene 15 affects the sensitivity of hepatocellular carcinoma cells to norcantharidin