Prochlorperazine inhibits the proliferation of hepatocellular carcinoma cells by promoting phosphorylation of β-catenin.

Abstract

Hepatocellular carcinoma (HCC) is the most prevalent form of primary liver cancer and ranks as the third leading cause of cancer-related fatalities worldwide. Recently, prochlorperazine (PCZ), a synthetic antipsychotic medication, has gained attention for its potential anticancer properties. However, the specific mechanisms underlying its anticancer effects remain unclear. In this study, we have identified that PCZ effectively inhibits the proliferation of HCC cells and diminishes the number and size of HCC foci in the mouse model. Subsequent studies have revealed that PCZ can directly bind to β-catenin and enhance the phosphorylation level of β-catenin. This, in turn, inhibits the Wnt signaling pathway, thereby exerting its anticancer effects. This novel finding sheds light on the potential molecular mechanisms of PCZ as a therapeutic strategy for HCC. In summary, our study provides fresh insights into the utility of PCZ as a therapeutic option for HCC and elucidates its molecular mechanisms.