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肥胖与前列腺癌:脂肪因子的作用

Obesity and prostate cancer: a role for adipokines.

作者信息

Mistry Tina, Digby Janet E, Desai Ken M, Randeva Harpal S

机构信息

Molecular Medicine Research Group, Biomedical Research Institute, University of Warwick Medical School, Coventry, UK.

出版信息

Eur Urol. 2007 Jul;52(1):46-53. doi: 10.1016/j.eururo.2007.03.054. Epub 2007 Mar 26.

Abstract

OBJECTIVES

Many studies have investigated the association between obesity and prostate cancer risk but have yielded inconsistent results. Recent evidence suggests a particular role for obesity in prostate cancer progression. Many studies have investigated the roles of adipose tissue-derived factors (adipokines) as putative molecular mediators between obesity and prostate cancer. This review provides an overview of current evidence that supports such a role for adipokines.

METHODS

A comprehensive literature review was carried out using PubMed to search for articles relating to prostate cancer and the following adipokines: leptin, interleukin 6, vascular endothelial growth factor (VEGF), and adiponectin.

RESULTS

Prostate cancer cells are exposed to adipokines either via the circulation or through locally produced adipokines following invasion of the retropubic fat pad. Circulating levels of most adipokines are positively correlated with obesity; adiponectin is inversely correlated with obesity. High circulating levels of leptin, interleukin 6, and VEGF are associated with increased prostate cancer risk and increased aggressiveness. Adiponectin levels are lower in patients with prostate cancer and are inversely associated with grade of disease. Adipokines exert a variety of biologic effects on prostate cancer cells, modulating cellular differentiation, apoptosis, proliferation, and angiogenesis.

CONCLUSIONS

Evidence suggests a role for obesity and adipokines in promoting the progression of established prostate cancer. Adipokines may contribute to the molecular basis for the association between obesity and prostate cancer, but the complex pathophysiology of both these disease states requires further studies.

摘要

目的

许多研究已调查肥胖与前列腺癌风险之间的关联,但结果并不一致。近期证据表明肥胖在前列腺癌进展中具有特殊作用。许多研究已探讨脂肪组织衍生因子(脂肪因子)作为肥胖与前列腺癌之间假定分子介质的作用。本综述概述了支持脂肪因子发挥此类作用的当前证据。

方法

使用PubMed进行全面的文献综述,以搜索与前列腺癌及以下脂肪因子相关的文章:瘦素、白细胞介素6、血管内皮生长因子(VEGF)和脂联素。

结果

前列腺癌细胞通过循环或在耻骨后脂肪垫受侵袭后通过局部产生的脂肪因子接触脂肪因子。大多数脂肪因子的循环水平与肥胖呈正相关;脂联素与肥胖呈负相关。瘦素、白细胞介素6和VEGF的高循环水平与前列腺癌风险增加和侵袭性增加相关。前列腺癌患者的脂联素水平较低,且与疾病分级呈负相关。脂肪因子对前列腺癌细胞发挥多种生物学作用,调节细胞分化、凋亡、增殖和血管生成。

结论

有证据表明肥胖和脂肪因子在促进已确诊前列腺癌的进展中发挥作用。脂肪因子可能是肥胖与前列腺癌之间关联的分子基础,但这两种疾病状态复杂的病理生理学需要进一步研究。

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