
Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16
Published: May 14, 2025
Introduction Valproic acid (VPA) constitutes a branched-chain, short-chain fatty that serves as an antiepileptic medication. It has been increasingly recognized VPA presented potential anti-tumor properties, including breast cancer. However, the exploration of novel cancer treatment methods necessitates more comprehensive and in-depth understanding mechanism inhibition proven farnesyl-diphosphate farnesyltransferase 1 (FDFT1) participate in oncogenesis development cancers. effect FDFT1 on is still obscure. Thus, it important to investigate trigger ferroptosis cells via targeting FDFT1. Methods In this study, underlying mechanisms were explored vitro vivo. Initially, effects proliferation assessed utilizing Cell Counting Kit-8, cell counting, colony formation assays. Subsequently, treated with determined through use Lipid Peroxidation malondialdehyde Assay Kit, reduced glutathione oxidized disulfide flow cytometry, transmission electron microscopy, western bloting. To explore impact combination ferrostatin-1, Erastin or RSL3, MDA-MB-231 ferroptosis, respective CCK-8, WB assays conducted. Thereafter, we whether facilitated by modulating expression Finally, anti-breast vivo validated xenograft mouse model, histological examination hematoxylin-eosin staining immunohistochemistry employed delve into VPA’s inhibitory Results Discussion The assay outcomes indicated impedes cells. findings from index demonstrated are sensitive induced than MCF-7 Subsequent introduction ferrostatin-1 (Fer-1), was observed Fer-1 reversed VPA, whereas conjunction respectively, We revealed downregulation enhanced inhibited Additionally, discovered may facilitate negatively levels solute carrier family 7 member 11 (SLC7A11) protein upregulation expression. conclusion, study elucidated FDFT1, representing its efficacy potentially inhibiting
Language: Английский