The relationship of obesity and prostate cancer (review)
Obesity is a critical risk factor for prostate cancer (PCa). Adipose tissue plays an important role in tumor development, including growth, invasion, and metastasis. Diet and dietary components affect the progression of prostate cancer; however, the mechanisms underlying these associations remain unclear. Extraprostatic prostate tumor cells form a new microenvironment in the periprostatic adipose tissue, which alters these interactions and promotes tumor progression. Hyperinsulinemia leads to an increase in the level of free or biologically active insulin-like growth factor (IGF-1) due to a decrease in the production of IGF-binding proteins. Hypoandrogenism promotes the development of a more aggressive type of prostate cancer (higher Gleason scores). Adipokines of adipose tissue and cytokines (for example, interleukin-6 (IL-6) and tumor necrosis factor (TNF-), angiogenic factors (for example, vascular endothelial growth factor (VEGF), apelin (AGTRL1) and other factors (for example, leptin and adiponectin) have multiple effects on prostate cancer cells. Tumor cells interact directly or indirectly with adipocytes. Yellow (inactive) bone marrow is adipose tissue with separate islands of reticular tissue. It is located in the medullary canals of the tubular bones and in parts of the cells of the cancellous bone. Bone tissue is the object of the most frequent metastasis in prostate cancer, and with age, the content of fat cells in it increases. Bone marrow adipose tissue interacts with tumor cells, osteoblasts and other stromal cells and participates in the organization of the tumor microenvironment. Adipokines are key molecules in the interaction between tumor cells and adipose tissue, which is carried out through various mechanisms. A better understanding of the role of adipose tissue in the induction and progression of prostate cancer will lead to effective therapeutic strategies for this disease.