Rhee Handoo, Vela Ian, Chung Eric
Department of Urology, Princess Alexandra Hospital, University of Queensland, Brisbane, QLD, Australia.
Australian Prostate Cancer Research Centre-Queensland, Princess Alexandra Hospital, Brisbane, QLD, Australia.
Horm Cancer. 2016 Apr;7(2):75-83. doi: 10.1007/s12672-015-0238-x. Epub 2015 Nov 6.
The human prostate gland is an endocrine organ where dysregulation of various hormonal factors may play a pivotal role in the pathogenesis of prostate cancer. There is emerging epidemiological data to support the role of components of metabolic syndrome, namely, obesity, hypercholesterolaemia, diabetes and hyperinsulinaemia on the development and/or the progression of prostate cancer. Although the exact mechanisms behind the relationship between metabolic syndrome and prostate cancer remain largely unknown, various in vitro and animal experiments of metabolic syndrome models have been shown to promote survival, mitogenesis, metastasis and treatment resistance pathways, through various adaptive responses such as intracellular steroidogenesis and lipogenesis. Also, in a large proportion of men with metabolic syndrome, alteration in levels of hormones such as testosterone, leptin and adiponectin has been shown to contribute towards the aggression of prostate cancer. Whilst the exact bio-pathophysiological mechanisms between metabolic syndrome and prostate cancer are yet to be fully elucidated, medications that target specific components of metabolic syndrome have further provided evidence for the inter-relationship between metabolic syndrome, its components and prostate cancer. Emerging in vitro and molecular data is likely to bring us closer to utilizing this knowledge to target particular cancer survival pathways and improving outcomes for men with prostate cancer.
人类前列腺是一个内分泌器官,各种激素因子的失调可能在前列腺癌的发病机制中起关键作用。越来越多的流行病学数据支持代谢综合征的组成部分,即肥胖、高胆固醇血症、糖尿病和高胰岛素血症在前列腺癌发生和/或进展中的作用。尽管代谢综合征与前列腺癌之间关系背后的确切机制仍大多未知,但代谢综合征模型的各种体外和动物实验已表明,通过细胞内类固醇生成和脂肪生成等各种适应性反应,可促进生存、有丝分裂、转移和治疗抵抗途径。此外,在很大一部分患有代谢综合征的男性中,睾酮、瘦素和脂联素等激素水平的改变已被证明会促使前列腺癌恶化。虽然代谢综合征与前列腺癌之间确切的生物病理生理机制尚未完全阐明,但针对代谢综合征特定组成部分的药物进一步为代谢综合征及其组成部分与前列腺癌之间的相互关系提供了证据。新出现的体外和分子数据可能会让我们更接近利用这些知识来靶向特定的癌症生存途径,并改善前列腺癌男性患者的治疗效果。