Abstract
Cholesterol metabolism has been extensively studied for its role in cell replication and growth (1). Besides the fact that cholesterol is a constitutive physiological compound of plasma membranes, it is believed that intermediate molecules of its metabolism are directly implied with DNA synthesis (2). Several experimental reports support these assumptions. The following general considerations can be recalled:
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1.
A “continuous” flow of cholesterol synthesis is needed during cell proliferation in order to supply the cholesterol required for biogenesis of new membranes that must accompany cell growth (3).
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2.
The pioneering work of Siperstein showed the loss of feedback inhibition by cholesterol on hydroxy-methyl-glutaryl coenzyme A (HMGCoA) reductase in tumoral tissue (4).
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3.
In the last decade different Authors have repeatedly given “in vitro” experimental evidence that isoprenoid units are directly correlated with DNA synthesis (5–7).
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4.
Cholesterol synthesis and correlated metabolic pathways (hexose monophosphate (HMP) shunt, cholesterol esterification, lipoprotein metabolism) are synchronized with DNA synthesis and with the extent of parenchymal cell proliferation (8–12).
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© 1988 Plenum Press, New York
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Pani, P., Dessì, S., Batetta, B. (1988). Cholesterol Metabolism During Cell Proliferation. In: Roberfroid, M.B., Préat, V. (eds) Experimental Hepatocarcinogenesis. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0957-4_15
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DOI: https://doi.org/10.1007/978-1-4613-0957-4_15
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