{"title":"Curcumin inhibits growth and triggers apoptosis in human castration-resistant prostate cancer cells via IGF-1/PI3K/Akt pathway.","authors":"Chao Chen, Qiwu Wang, Jiwen Liu","doi":"10.1177/03000605231220807","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate the possible mechanism by which curcumin inhibits human prostate cancer (PCa) and castration-resistant prostate cancer (CRPC).</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>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.</p>","PeriodicalId":16129,"journal":{"name":"Journal of International Medical Research","volume":"53 2","pages":"3000605231220807"},"PeriodicalIF":1.4000,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11806470/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of International Medical Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1177/03000605231220807","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0
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.
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