Anticancer activities of sulindac in prostate cancer cells associated with c-Jun NH2-terminal kinase 1/β-catenin signaling

Abstract

The non-steroidal anti-inflammatory agent, sulindac, has shown strong effects on cancer prevention in colorectal cancers, however, its anticancer activities on prostate cancer remain unclear. In the current study, human prostate cancer cell lines, LNCaP and PC-3, were treated with various concentrations of sulindac and it was found that sulindac significantly inhibits prostate cancer cell proliferation and promotes cell apoptosis in a dose- and time-dependent manner. Further studies revealed that sulindac significantly induces c-Jun NH2-terminal kinase (JNK)phosphorylation and inhibits β-catenin at the transcriptional and post-transcriptional levels. In conclusion, by targeting the JNK1/β-catenin signaling pathway, sulindac may present a potential preventive or therapeutic agent for treatment of patients with prostate cancer.