Biochemical and Biophysical Research Communications
Regular ArticleInhibition of Isoprenoid Biosynthesis Induces Apoptosis in Human Promyelocytic HL-60 Cells
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Role of cholesterol metabolism in the anticancer pharmacology of selective estrogen receptor modulators
2021, Seminars in Cancer BiologyCitation Excerpt :In human leukemia cells incubated in a medium free of cholesterol and mevalonic acid, the effects of statins on cell viability and cell cycle distribution greatly depend on the dose used. With supratherapeutic doses (≥ 50 μM lovastatin), which blocked both cholesterol biosynthesis and protein prenylation [103], massive apoptosis occurred and the proportion of cells accumulating in G0/G1 highly increased to the detriment of the active S and G2/M phases [101,103,116,117]. This effect was independent of p53 status as the addition of exogenous mevalonate prompted cells arrested at G1 to progress through the S phase and reach G2/M [103].
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2020, BoneCitation Excerpt :Although this observation perhaps received little attention at the time, it became more relevant several years later when N-BPs were recognised to cause cell death by apoptosis [24,44]. Disruption of the mevalonate pathway by statins (Fig. 4) had also been found to cause apoptosis, by preventing the production of isoprenoid lipids necessary for protein prenylation [45]. Prenylation, explained in more detail below, is a type of protein modification essential in all cells for the membrane targeting and normal function of many proteins, particularly small GTPases such as those of the Rho, Rac and Rab families.
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