Conclusions

We have summarized a large literature that points to a role for cholesterol in PCa progression. The evidence for this conclusion arises from epidemiology studies suggesting that a Western diet can promote, and long-term treatment with cholesterol-lowering drugs can inhibit, PCa growth. These findings in humans are supported by an array of molecular biological studies that point to a role for membrane cholesterol in cell signaling mechanisms relevant to PCa progression. Much of the data in the literature can be interpreted through the paradigm of the lipid raft model (diagrammed in Fig. 3), in which cholesterol-rich domains serve to process biochemical signals for tumor cell survival, proliferation, and migration. This model also accounts for the descriptive findings discussed here that suggest that malignant growth and cancer progression coincide with local tissue alterations in fat metabolism, and in particular, accumulation of cholesterol in tumor cell membranes. Further study of cholesterol-enriched microdomains in the context of cell signaling mechanisms will lead to new avenues for therapeutic intervention in PCa and other malignancies.

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