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  • Title: Induction of apoptosis in p53-null HL-60 cells by inhibition of lanosterol 14-alpha demethylase.
    Author: Martínez-Botas J, Ferruelo AJ, Suárez Y, Gómez-Coronado D, Lasunción MA.
    Journal: Biochimie; 1998 Nov; 80(11):887-94. PubMed ID: 9893947.
    Abstract:
    To determine the role of cholesterol deprivation in cell proliferation and, eventually, in apoptosis, HL-60 promyelocytic cells were incubated in a cholesterol-depleted medium in the presence of SKF 104976, a specific inhibitor of lanosterol 14-alpha demethylase. As expected, SKF 104976 efficiently blocked the [14C]-acetate incorporation into cholesterol, whereas it induced the accumulation of both lanosterol and, especially, dihydrolanosterol. As a consequence, cell proliferation was greatly depressed at 24 h of treatment with the drug, and clear signs of apoptosis--annexin V binding, condensed and fragmented nuclei and DNA ladder--were observed thereafter. Provided that the HL-60 cell line does not express p53, it may be concluded that apoptosis induced by cholesterol deprivation is not dependent on this tumor suppressor protein. Supplementing the incubation medium with LDL-cholesterol or pure free cholesterol, fully prevented cell growth inhibition and apoptosis induction, whereas mevalonate was ineffective. These results indicate that cholesterol plays a specific role in cell proliferation, a function that is not shared by its precursors lanosterol and dihydrolanosterol.
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