Abstract
Simple SummaryProstate cancer presents a significant global public health burden. One of its established risk factors is high fat diet. It has been proven that cholesterol levels in blood and prostate tissue are out of balance, while cholesterol metabolism in prostate cancer is deregulated and plays an important role in cancer progression. In this review we have shown the connection between commonly deregulated pathways in prostate cancer and cholesterol metabolism.Prostate cancer (PC) is the most common malignancy in men. Common characteristic involved in PC pathogenesis are disturbed lipid metabolism and abnormal cholesterol accumulation. Cholesterol can be further utilized for membrane or hormone synthesis while cholesterol biosynthesis intermediates are important for oncogene membrane anchoring, nucleotide synthesis and mitochondrial electron transport. Since cholesterol and its biosynthesis intermediates influence numerous cellular processes, in this review we have described cholesterol homeostasis in a normal cell. Additionally, we have illustrated how commonly deregulated signaling pathways in PC (PI3K/AKT/MTOR, MAPK, AR and p53) are linked with cholesterol homeostasis regulation.
Highlights
Prostate cancer (PC) with high incidence (>1.1 million new cases each year) and mortality (~300,000 deaths per year) presents a significant global public health burden [1,2].Established risk factors of PC are age, race and family history of disease [3,4]
Many studies have shown that cholesterol and low-density lipoprotein (LDL) are significantly higher in PC and men with hypercholesterolemia are usually at higher risk of developing high-grade PC [72,73,74]
Inter-individual genetic variability could contribute to confusing epidemiological results. 17 genomic locations associated with PC are associated with LDL and triglycerides while there were no pleotropic loci shared between
Summary
Prostate cancer (PC) with high incidence (>1.1 million new cases each year) and mortality (~300,000 deaths per year) presents a significant global public health burden [1,2]. Established risk factors of PC are age, race and family history of disease [3,4]. Many risk factors are non-modifiable, association with preventable high fat diets, risk of PC and progression of the disease have been observed in different studies [5,6,7,8,9]. High fat diet increases total and low-density lipoprotein (LDL) cholesterol and decreases high-density lipoprotein (HDL) cholesterol in plasma [10]. Experiments on cell culture, xenografts, clinical samples and epidemiological studies confirm aberrant cholesterol metabolism in PC and its importance in progression [11,12,13]. We summarized current knowledge related to cholesterol metabolism and its function in normal cells. We illustrated how commonly deregulated signaling pathways in PC reflect cholesterol metabolism
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