Effects of aspirin on hepatocellular carcinoma and its potential molecular mechanism

To explore the effects of aspirin (ASP) on the proliferation and apoptosis of HepG2 hepatocellular carcinoma (HCC) cells via the Wnt/β-catenin signaling pathway.

Human HCC cells were cultured and treated with ASP at different concentrations. Cell proliferation was determined with cell counting kit-8 (CCK-8) and colony formation, and the rate of apoptosis was measured by flow cytometry. Western blotting (WB) and quantitative polymerase chain reaction (qRT-PCR) assays were used to assess the changes in the expression levels of related proteins.

ASP showed a time-and concentration-depented inhibitory effect on HepG2 cell proliferation. The number of colonies formed in ASP-treated HCC cells was significantly lower than in control cells. For HCC cells treated with ASP, the apoptosis rate enhanced with the increase of ASP concentration. The expression levels of TCF4 and LEF1, key molecules of the Wnt/β-catenin signaling pathway, were lowered in HCC cells treated with 4 mM ASP, and the nuclear translocation of β-catenin was weakened. The β-catenin activator exerted a negative influence on the anticancer effect of ASP.

ASP inhibits the proliferation and promotes the apoptosis of HCC cells through the Wnt/β-catenin signaling pathway.