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Polyoxometalates (POMs) exhibit unique structural characteristics and excellent physical and chemical properties, which have attracted significant attention from scholars in the fields of anticancer research and chemotherapy. Herein, we successfully synthesized and structurally characterized two novel polyoxovanadates (POVs), denoted as POVs-1 and POVs-2, where [M(1-vIM)4]2[VV4O12]·H2O (M: NiII and MnII, 1-vinylimidazole abbreviated as 1-vIM) serve as ligands. The two POVs are isomeric and consist of fundamental structural units, each comprising one [V4O12]4− cluster, two [M(1-vIM)4]2+ cations, and one water molecule. Subsequently, we evaluated the cell viability of human hepatocellular carcinoma (HepG-2) cells treated with the synthesized POVs using the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazoliumbromide) assay. And the changes in cell nucleus morphology, mitochondrial membrane potential (Δψm), and reactive oxygen species levels in HepG-2 exposed to POVs were monitored using specific fluorescent staining techniques. Both hybrid POVs showed potent inhibitory activities, induing apoptosis in HepG-2 cells along with significant mitochondria dysfunction and a burst of reactive oxygen species. Notably, the inhibitory effects of POVs-2 were more pronounced than those of POVs-1, which is primarily attributed to the different transition metal ions present. These findings underscore the intricate relationship between the metal components, structural characteristics, and the observed antitumor activities in HepG-2 cells. [ABSTRACT FROM AUTHOR]

Abstract: Apoptosis of vascular smooth muscle cell (VSMC) is one of the major pathologic features in atherosclerosis. The platelet-derived growth factor (PDGF) pathway has been shown to provide survival signals in VSMCs and PDGF receptors are also highly expressed in VSMCs contained in the plaques of atherosclerosis. However, the downstream targets of PDGF signaling are unclear. In the current study, we show that PDGF signals stimulate the protein expression of c-Myb in human arterial VSMCs. Inhibition of c-Myb function in VSMCs enhanced apoptosis in PDGF treated VSMCs. Our data suggest that c-Myb functions as a downstream target of the PDGF survival pathway and suggest that c-Myb plays an essential role in adult VSMC survival. [Copyright &y& Elsevier]