18 research outputs found
Nucleotide sequence of the ERG12 gene of Saccharomyces cerevisiae encoding mevalonate kinase
Chinese hamster cell mutant resistant to ML236B (Compactin) is defective in endocytosis of low-density lipo-protein
The effect of mevalonate on 3-hydroxy-3-methylglutaryl-CoA reductase activity and the absolute rate of cholesterol biosynthesis in human monocyte-derived macrophages
Squalene Does Not Exhibit a Chemopreventive Activity and Increases Plasma Cholesterol in a Wistar Rat Hepatocarcinogenesis Model
p53 regulates the mevalonate pathway in human glioblastoma multiforme
The mevalonate (MVA) pathway is an important metabolic pathway implicated in multiple aspects of tumorigenesis. In this study, we provided evidence that p53 induces the expression of a group of enzymes of the MVA pathway including 3′-hydroxy-3′- methylglutaryl-coenzyme A reductase, MVA kinase, farnesyl diphosphate synthase and farnesyl diphosphate farnesyl transferase 1, in the human glioblastoma multiforme cell line, U343 cells, and in normal human astrocytes, NHAs. Genetic and pharmacologic perturbation of p53 directly influences the expression of these genes. Furthermore, p53 is recruited to the gene promoters in designated p53-responsive elements, thereby increasing their transcription. Such effect was abolished by site-directed mutagenesis in the p53-responsive element of promoter of the genes. These findings highlight another aspect of p53 functions unrelated to tumor suppression and suggest p53 as a novel regulator of the MVA pathway providing insight into the role of this pathway in cancer progression