作者: Norbert Bakalara , Jan de Weille , Christine Fabre
DOI: 10.1016/J.BCP.2013.02.029
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摘要: Oxysterols have been shown to interfere with proliferation and cause the death of many cancer cell types, such as leukaemia, glioblastoma, colon, breast prostate cells, while they little or no effect on senescent cells. The mechanisms by which oxysterols may influence are manifold: control transcription turnover key enzyme in cholesterol synthesis, 3-hydroxy-3-methylglutaryl CoA reductase, binding Insig-1, Insig-2 liver X receptors. thought be generated proportion rate synthesis. Although there is consensus about mechanism these vivo, it clearly has ubiquitous. 25- 27-cholesterol hydroxylases, present almost all tissues, possible candidates. Cholesterol uptake from lipoproteins, intracellular vesicle transport lipid transfer also modified oxysterols. ERK, hedgehog wnt pathways differentiation. When administered vitro lines, invariably both slow down provoke death. Perhaps sufficient stop a its eradication. Therefore, two facets oxysterol action that seem important for treatment, cytostaticity cytotoxicity, will discussed.