Abstract

Prostate cancer is the second most common cancer affecting the male population all over the world. The existence of a correlation between lipid metabolism disorders and cancer of the prostate gland has been widely known for a long time. According to hypotheses, cholesterol may contribute to prostate cancer progression as a result of its participation as a signaling molecule in prostate growth and differentiation via numerous biologic mechanisms including Akt signaling and de novo steroidogenesis. The results of some studies suggest that increased cholesterol levels may be associated with a higher risk of a more aggressive course of the disease. The aforementioned alterations in the synthesis of fatty acids are a unique feature of cancer and, therefore, constitute an attractive target for therapeutic intervention in the treatment of prostate cancer. Pharmacological or gene therapy aims to reduce the activity of enzymes involved in de novo synthesis of fatty acids, FASN, ACLY (ATP citrate lyase) or SCD-1 (Stearoyl-CoA Desaturase) in particular, that may result in cells growth arrest. Nevertheless, not all cancers are unequivocally associated with hypocholesterolaemia. It cannot be ruled out that the relationship between prostate cancer and lipid disorders is not a direct quantitative correlation between carcinogenesis and the amount of circulating cholesterol. Perhaps the correspondence is more sophisticated and connected to the distribution of cholesterol fractions or even sub-fractions of e.g. HDL cholesterol.

Keywords: Prostate cancer, carcinogenesis, cholesterol levels, lipids disorders, metastasis, cells growth, gene therapy.