Min Liu, Chuanbing Xu, Huichao Dong, Dongsheng Jia, Dongfang Hao, Ruozen Rong, Yao Peng
{"title":"Iron Oxide Nanoparticles Carrying microRNA-124 Promote Ferroptosis in Treatment of Prostate Cancer","authors":"Min Liu, Chuanbing Xu, Huichao Dong, Dongsheng Jia, Dongfang Hao, Ruozen Rong, Yao Peng","doi":"10.1166/jbn.2024.3782","DOIUrl":null,"url":null,"abstract":"Prostate cancer (PCa) is a common malignancy among men worldwide. Iron oxide (Fe3O4) nanoparticles (NPs) exhibit great potential in gene delivery and studies have noted the inhibitory effect of miR-124 on PCa cell growth. Herein, we identified the therapeutic effect\n of Fe3O4 NPs carrying miR-124 in PCa and clarified its mechanism of action in inhibiting progression of PCa. After preparation of Fe3O4 NPs carrying miR-124, human PCa cell line PC3 was treated with miR-124-Fe3O4 NPs when ferroptosis\n inducer FIN56, ferroptosis inhibitor Liproxstatin-1, Phosphatase and tensin homolog (PTEN) inhibitor SF1670 or PTEN activator Oroxin B were added for transfection. Afterwards, assays were conducted to evaluate PCa cell biological activities. Additionally, we determined expression of PTEN and\n AKT and ferroptosis-related protein GPX4 and SLC7A11 in each group. We confirmed anticancer effects of miR-124-Fe3O4 NPs in PCa, as they suppressed PC3 cell proliferation and migration, and induced apoptosis. Compared with miR-124-Fe3O4 + Liproxstatin-1\n group, the expressions of GPX4 and SLC7A11 proteins in miR-124-Fe3O4 group were elevated. The advent of PTEN activator Oroxin B decreased proliferative ability of PCa cells, and SF1670 treatment decreased PTEN level and elevated AKT level. With highest apoptotic rate\n of PCa cells in miR-124-Fe3O4 + Oroxin B + FIN56 group, intervention of SF1670 or Liproxstatin-1 changed the cell viability, while Oroxin B caused decreased AKT level and increased level of ferroptosis-related proteins. miR-124-Fe3O4 NPs hinder PCa\n progression by promoting ferroptosis and cell apoptosis through regulation of PTEN/Akt pathway.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9000,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of biomedical nanotechnology","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1166/jbn.2024.3782","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
Prostate cancer (PCa) is a common malignancy among men worldwide. Iron oxide (Fe3O4) nanoparticles (NPs) exhibit great potential in gene delivery and studies have noted the inhibitory effect of miR-124 on PCa cell growth. Herein, we identified the therapeutic effect
of Fe3O4 NPs carrying miR-124 in PCa and clarified its mechanism of action in inhibiting progression of PCa. After preparation of Fe3O4 NPs carrying miR-124, human PCa cell line PC3 was treated with miR-124-Fe3O4 NPs when ferroptosis
inducer FIN56, ferroptosis inhibitor Liproxstatin-1, Phosphatase and tensin homolog (PTEN) inhibitor SF1670 or PTEN activator Oroxin B were added for transfection. Afterwards, assays were conducted to evaluate PCa cell biological activities. Additionally, we determined expression of PTEN and
AKT and ferroptosis-related protein GPX4 and SLC7A11 in each group. We confirmed anticancer effects of miR-124-Fe3O4 NPs in PCa, as they suppressed PC3 cell proliferation and migration, and induced apoptosis. Compared with miR-124-Fe3O4 + Liproxstatin-1
group, the expressions of GPX4 and SLC7A11 proteins in miR-124-Fe3O4 group were elevated. The advent of PTEN activator Oroxin B decreased proliferative ability of PCa cells, and SF1670 treatment decreased PTEN level and elevated AKT level. With highest apoptotic rate
of PCa cells in miR-124-Fe3O4 + Oroxin B + FIN56 group, intervention of SF1670 or Liproxstatin-1 changed the cell viability, while Oroxin B caused decreased AKT level and increased level of ferroptosis-related proteins. miR-124-Fe3O4 NPs hinder PCa
progression by promoting ferroptosis and cell apoptosis through regulation of PTEN/Akt pathway.