Curcumin inhibits growth and triggers apoptosis in human castration-resistant prostate cancer cells via IGF-1/PI3K/Akt pathway

J Int Med Res. 2025 Feb;53(2):3000605231220807. doi: 10.1177/03000605231220807.

Abstract

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

Methods: 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.

Results: 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.

Keywords: Curcumin; anti-cancer; castration-resistant prostate cancer; insulin-like growth factor-1; phosphoinositide 3-kinase; protein kinase B; signaling pathway.

MeSH terms

  • Apoptosis* / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Curcumin* / pharmacology
  • Forkhead Box Protein O1 / metabolism
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Insulin-Like Growth Factor I* / genetics
  • Insulin-Like Growth Factor I* / metabolism
  • Male
  • Phosphatidylinositol 3-Kinases* / genetics
  • Phosphatidylinositol 3-Kinases* / metabolism
  • Prostatic Neoplasms, Castration-Resistant* / drug therapy
  • Prostatic Neoplasms, Castration-Resistant* / genetics
  • Prostatic Neoplasms, Castration-Resistant* / metabolism
  • Prostatic Neoplasms, Castration-Resistant* / pathology
  • Proto-Oncogene Proteins c-akt* / genetics
  • Proto-Oncogene Proteins c-akt* / metabolism
  • Receptor, IGF Type 1 / genetics
  • Receptor, IGF Type 1 / metabolism
  • Signal Transduction* / drug effects

Substances

  • Curcumin
  • Proto-Oncogene Proteins c-akt
  • Insulin-Like Growth Factor I
  • Phosphatidylinositol 3-Kinases
  • Receptor, IGF Type 1
  • IGF1 protein, human
  • IGF1R protein, human
  • Forkhead Box Protein O1