Previous epidemiological studies have pointed to an association between low serum cholesterol levels and the incidence of gastro-intestinal cancers, in particular colorectal cancer [129]. This topic is still controversial [130,131]. However, this data taken together with the increasing evidence that statins can act as immunomodulators, in both animal models and in vitro, and the role of statins in reversing hypoxic inhibition of eNOS, thereby promoting increased local blood flow through eNOS activity, have raised concerns over the long term use of statins in terms of immune surveillance for tumours. However, large scale prolonged clinical trials have given no evidence for an association of statin use with cancer [132].

As discussed above, statins have been shown to cause cell cycle arrest and induce apoptosis of VSMC through the inhibition of geranylgeranylation of Rho, thereby dis-inhibiting the effect of Rho on Cdk inhibitors, p21 andp27 [7-9,74,75]. The role of Rho-family proteins in mediating intracellular signalling pathways involved in cell cycle progression, cytokinesis and cell migration/motility makes this family an attractive target for oncology [7-9,133,134]. Thus, the potential for statins to interfere with the isoprenylation of Rho-family proteins in cells has been studied and a number of observations reported that indicate that statins in vitro cause cell cycle arrest and change the behaviour of cells in invasion models such as Boyden chambers [135,136].

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