ArticleMolecular biology reports2025
Investigation of the antitumor effects of deferasirox on prostate cancer cells: insights into proliferation, apoptosis, and invasion mechanisms.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionThis study was conducted to determine whether DFX (deferasirox) exhibits antitumor activity in prostate cancer cell lines. Iron is a vital element for cellular proliferation, growth, and metabolism. However, both iron overload and altered iron metabolism have been associated with tumor initiation and progression. DFX is an orally administered iron chelator, which makes its therapeutic application more convenient compared to other chelators administered via parenteral routes. Although some studies have suggested that DFX is a promising candidate for cancer prevention and treatment, its efficacy against prostate cancer cells has not yet been fully elucidated. Iron deprivation may represent a novel therapeutic strategy for cancer. MATERIAL AND
methodsThe antitumor effects of DFX were evaluated through cell viability, invasion, cell cycle, and apoptosis assays, along with gene and protein expression analyses related to metastasis.
resultsThe results demonstrated that DFX reduced cell viability in PC3 and LNCaP prostate cancer cell lines. In the normal prostate epithelial cell line PNT1A, this effect was observed only at higher IC₅₀ doses. Treatment of PC3 and LNCaP cell lines with the determined IC₅₀ concentrations of DFX resulted in cell cycle arrest and a marked reduction in migratory potential. Moreover, the mRNA expression of NDRG1, a known anti-metastatic marker, was upregulated. However, increased protein expression was evident only in PC3 cells, while no significant increase was detected in LNCaP cells.
conclusionsThis study highlights the potential of DFX as an effective anticancer agent in the treatment of prostate cancer.
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