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The human prostate gland is an endocrine organ in which dysregulation of various hormonal factors plays a key role in the development of non-tissue transformation and leads to the formation of prostate cancer. Existing epidemiological data confirm the role of the components of the metabolic syndrome, namely obesity, hypercholesterolemia, diabetes, and hyperinsulinemia, in the development and/or progression of prostate cancer. Although the exact mechanisms underlying the relationship between metabolic syndrome and prostate cancer remain largely unknown, it has been shown that various “in vitro” and animal experiments with models of the metabolic syndrome contribute to survival, mitogenesis, metastasis, and treatment resistance pathways through various adaptive reactions, such as intracellular steroidogenesis and lipogenesis. Although the exact biopathophysiological mechanisms between metabolic syndrome and prostate cancer have yet to be studied, drugs that target specific components of the metabolic syndrome have also provided evidence for the relationship between metabolic syndrome, its components, and prostate cancer. The appearance of “in vitro” results and molecular genetic research data will bring us closer to using this knowledge to determine specific ways of cancer-specific survival and improve treatment outcomes in patients with this disease.