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本文引用的文献

1
Human Cancer Cells Signal Their Competitive Fitness Through MYC Activity.人类癌细胞通过 MYC 活性来传递其竞争适应性。
Sci Rep. 2017 Oct 3;7(1):12568. doi: 10.1038/s41598-017-13002-1.
2
Reversal of hyperactive Wnt signaling-dependent adipocyte defects by peptide boronic acids.肽硼酸逆转 Wnt 信号过度激活导致的脂肪细胞缺陷
Proc Natl Acad Sci U S A. 2017 Sep 5;114(36):E7469-E7478. doi: 10.1073/pnas.1621048114. Epub 2017 Aug 21.
3
Control of intestinal stem cell function and proliferation by mitochondrial pyruvate metabolism.线粒体丙酮酸代谢对肠道干细胞功能和增殖的调控
Nat Cell Biol. 2017 Sep;19(9):1027-1036. doi: 10.1038/ncb3593. Epub 2017 Aug 14.
4
Activin signaling mediates muscle-to-adipose communication in a mitochondria dysfunction-associated obesity model.在与线粒体功能障碍相关的肥胖模型中,激活素信号传导介导肌肉与脂肪之间的通讯。
Proc Natl Acad Sci U S A. 2017 Aug 8;114(32):8596-8601. doi: 10.1073/pnas.1708037114. Epub 2017 Jul 24.
5
Reprogramming glucose metabolism in cancer: can it be exploited for cancer therapy?重编程癌症中的葡萄糖代谢:能否将其用于癌症治疗?
Nat Rev Cancer. 2016 Oct;16(10):635-49. doi: 10.1038/nrc.2016.77. Epub 2016 Sep 16.
6
In vivo genetic dissection of tumor growth and the Warburg effect.肿瘤生长与瓦伯格效应的体内遗传学剖析
Elife. 2016 Sep 1;5:e18126. doi: 10.7554/eLife.18126.
7
Body Fatness and Cancer--Viewpoint of the IARC Working Group.身体肥胖与癌症——国际癌症研究机构工作组的观点
N Engl J Med. 2016 Aug 25;375(8):794-8. doi: 10.1056/NEJMsr1606602.
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High fat diet-induced TGF-β/Gbb signaling provokes insulin resistance through the tribbles expression.高脂饮食诱导的转化生长因子-β/糖原合酶激酶信号通路通过TRIBbles表达引发胰岛素抵抗。
Sci Rep. 2016 Aug 3;6:30265. doi: 10.1038/srep30265.
9
Survival of the Fittest: Essential Roles of Cell Competition in Development, Aging, and Cancer.适者生存:细胞竞争在发育、衰老和癌症中的重要作用。
Trends Cell Biol. 2016 Oct;26(10):776-788. doi: 10.1016/j.tcb.2016.05.009. Epub 2016 Jun 16.
10
Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy.肥胖诱导的炎症和促结缔组织增生促进胰腺癌进展及化疗耐药。
Cancer Discov. 2016 Aug;6(8):852-69. doi: 10.1158/2159-8290.CD-15-1177. Epub 2016 May 31.

果蝇作为研究新陈代谢与癌症之间联系的模型。

Drosophila as a Model to Study the Link between Metabolism and Cancer.

作者信息

Herranz Héctor, Cohen Stephen M

机构信息

Department of Cellular and Molecular Medicine, University of Copenhagen, Blegdamsvej 3, 2200 N Copenhagen, Denmark.

出版信息

J Dev Biol. 2017 Dec 1;5(4):15. doi: 10.3390/jdb5040015.

DOI:10.3390/jdb5040015
PMID:29615570
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5831792/
Abstract

Cellular metabolism has recently been recognized as a hallmark of cancer. Investigating the origin and effects of the reprogrammed metabolism of tumor cells, and identifying its genetic mediators, will improve our understanding of how these changes contribute to disease progression and may suggest new approaches to therapy. is emerging as a valuable model to study multiple aspects of tumor formation and malignant transformation. In this review, we discuss the use of as model to study how changes in cellular metabolism, as well as metabolic disease, contribute to cancer.

摘要

细胞代谢最近已被公认为癌症的一个标志。研究肿瘤细胞重编程代谢的起源和影响,并确定其遗传介质,将增进我们对这些变化如何促进疾病进展的理解,并可能提示新的治疗方法。正成为研究肿瘤形成和恶性转化多个方面的有价值模型。在本综述中,我们讨论使用作为模型来研究细胞代谢变化以及代谢疾病如何促成癌症。