ABSTRACT
Hepatocellular carcinoma (HCC) has high morbidity and mortality, and effective therapies are lacking. Gallic acid (GA), a natural phenolic compound derived from plants, has been reported to prevent the onset and progression of various cancers. However, there is limited elaboration on the potential mechanisms and anticancer effects of GA on hepatocellular carcinoma. Inducing ferroptosis of tumor cells has become one of the most promising ways to eradicate tumor cells. However, the effect of GA on HCC ferroptosis remains unknown. We evaluated the impact of GA on cell viability, migration, and mitochondrial morphology in HepG2 cells. Our study identified a critical role of GA in inducing ferroptosis in HepG2 cells. Mechanistically, we found that GA could inhibit the expression of a ferroptosis-related protein SLC7A11 and GPX4 in HepG2, by blocking ß-catenin transport from nuclear to the cytoplasm, thus inducing the inactivation of the Wnt/ß-catenin pathway. Our study has confirmed that GA is a novel ferroptosis inducer of HC, suggesting GA could be a promising candidate for the clinical treatment of HCC.
Subject(s)
Carcinoma, Hepatocellular , Ferroptosis , Liver Neoplasms , Humans , Carcinoma, Hepatocellular/pathology , Liver Neoplasms/pathology , beta Catenin/metabolism , Wnt Signaling Pathway , Cell Line, Tumor , Cell Proliferation , Gene Expression Regulation, NeoplasticABSTRACT
In this study, we present a nickel-catalyzed reductive C(sp3)-Sb coupling of unactivated alkyl chlorides with chlorostibines. This approach is highly versatile, tolerating various functional groups such as acetal, alkene, nitrile, amine, ester, silyl ether, thioether, and various heterocyclic compounds. Notably, the late-stage modification of bioactive molecules and the satisfactory anticancer activity against cancerous MDA-MB-231 also demonstrate the potential application.
