Hirabayashi Susumu
Metabolism and Cell Growth Group, MRC Clinical Sciences Centre (CSC), Du Cane Road, London W12 0NN, UK Institute of Clinical Sciences (ICS), Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, UK
Dis Model Mech. 2016 Sep 1;9(9):917-26. doi: 10.1242/dmm.025320.
Accumulating epidemiological evidence indicates a strong clinical association between obesity and an increased risk of cancer. The global pandemic of obesity indicates a public health trend towards a substantial increase in cancer incidence and mortality. However, the mechanisms that link obesity to cancer remain incompletely understood. The fruit fly Drosophila melanogaster has been increasingly used to model an expanding spectrum of human diseases. Fly models provide a genetically simpler system that is ideal for use as a first step towards dissecting disease interactions. Recently, the combining of fly models of diet-induced obesity with models of cancer has provided a novel model system in which to study the biological mechanisms that underlie the connections between obesity and cancer. In this Review, I summarize recent advances, made using Drosophila, in our understanding of the interplay between diet, obesity, insulin resistance and cancer. I also discuss how the biological mechanisms and therapeutic targets that have been identified in fly studies could be utilized to develop preventative interventions and treatment strategies for obesity-associated cancers.
越来越多的流行病学证据表明，肥胖与癌症风险增加之间存在密切的临床关联。肥胖的全球流行表明了一种公共卫生趋势，即癌症发病率和死亡率将大幅上升。然而，将肥胖与癌症联系起来的机制仍未完全明确。果蝇已越来越多地被用于模拟越来越多的人类疾病。果蝇模型提供了一个基因上更简单的系统，非常适合作为剖析疾病相互作用的第一步。最近，将饮食诱导肥胖的果蝇模型与癌症模型相结合，提供了一个新的模型系统，用于研究肥胖与癌症之间联系的生物学机制。在这篇综述中，我总结了利用果蝇在我们对饮食、肥胖、胰岛素抵抗和癌症之间相互作用的理解方面取得的最新进展。我还讨论了如何利用果蝇研究中确定的生物学机制和治疗靶点来制定肥胖相关癌症的预防干预措施和治疗策略。
