Post-lanosterol biosynthesis of cholesterol and cancer.

Mammalian cells require cholesterol for proliferation. Cholesterol contributes not only to the physicochemical properties of membranes but also to the organization of lipid rafts involved in signal transduction. Inhibition of cholesterol biosynthesis from lanosterol results in the inhibition of cell cycle progression and, in certain cell types, also in the induction of cell differentiation. Cholesterol metabolism, thus, appears to play a relevant role in the decision making between cell proliferation and differentiation. Several regulators of cholesterol metabolism, including certain microRNAs, are also involved in cell cycle regulation. The relevance of these processes in cancer underscores the interest for studying the role of cholesterol in tumorigenesis and exploring the possibility of interfering with the growth of malignant cells by manipulation of cholesterol metabolism.