ArticleMedical oncology (Northwood, London, England)2026
Mdivi-1 augments chlorpromazine's anticancer effect via modulation of mitochondrial dynamics, hallmarks of cancer-related cellular behavior, and oxidative stress.
Article in Medical oncology (Northwood, London, England), 2026. 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
The multifaceted therapeutic potential of phenothiazines was previously documented. This study investigated the anticancer effect of chlorpromazine (CPZ) in hepatoma and breast cancer cell lines and further explored the implications of mitochondrial dynamics. To establish this aim, the cytotoxic and antimitotic effects of CPZ combined with the mitochondrial fission inhibitor (mdivi-1) were assessed in HepG2 and MDA-MB-231 cells using MTT and clonogenic assays, respectively. Apoptosis and nuclear changes were evaluated with Annexin V/PI, acridine orange/ethidium bromide, and DAPI staining. Moreover, cell migration was examined using a wound-healing assay and the expression of epithelial-mesenchymal transition (EMT) markers. Additionally, 2',7'-dichlorodihydrofluorescein diacetate staining was used to assess cellular ROS, whereas the expression of mitochondrial fusion- and fission-related genes was assessed by RT-PCR. The results addressed CPZ's cytotoxic effect in both cancer cell types. The IC
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