These results demonstrated that curcumin inhibits growth and triggers apoptosis of human CRPC cells via the IGF-1/PI3K/Akt pathway, thus providing potential new therapeutic strategies for PCa and CRPC.

CRPC cells were treated with curcumin and their viability was assessed by MTT assay and apoptosis was detected by annexinV/propidium iodide double-staining and terminal deoxynucleotidyl transferase dUTP nick-end labeling assays. Expression levels of insulin-like growth factor 1 receptor (IGF-1R) were determined by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting. Phosphoinositide 3-kinase (PI3K), Akt, and forkhead box protein O1 (FOXO1) expression and phosphorylation were assessed by western blotting.

This study aimed to investigate the possible mechanism by which curcumin inhibits human prostate cancer (PCa) and castration-resistant prostate cancer (CRPC).

The highly expressed PCa-related molecule IGF-1R was down-regulated in CRPC cells after curcumin treatment, as determined by RT-qPCR and western blotting. In addition, curcumin inhibited the tumor-related PI3K/Akt signaling pathway in CRPC cells. Moreover curcumin down-regulated the IGF-1/PI3K/Akt signaling pathway in tumors derived from CRPC cells. Conclusions: These results demonstrated that curcumin inhibits growth and triggers apoptosis of human CRPC cells via the IGF-1/PI3K/Akt pathway, thus providing potential new therapeutic strategies for PCa and CRPC.