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乳腺癌代谢与线粒体活性:二甲双胍用于化学预防的可能性

Breast Cancer Metabolism and Mitochondrial Activity: The Possibility of Chemoprevention with Metformin.

作者信息

Cazzaniga Massimiliano, Bonanni Bernardo

机构信息

Division of Cancer Prevention and Genetics, European Institute of Oncology, 20141 Milan, Italy.

出版信息

Biomed Res Int. 2015;2015:972193. doi: 10.1155/2015/972193. Epub 2015 Oct 28.

Abstract

Metabolic reprogramming refers to the ability of cancer cells to alter their metabolism in order to support the increased energy request due to continuous growth, rapid proliferation, and other characteristics typical of neoplastic cells. It has long been believed that the increase of metabolic request was independent of the mitochondrial action but recently we know that mitochondrial activity together with metabolism plays a pivotal role in the regulation of the energy needed for tumor cell growth and proliferation. For these reasons the mitochondria pathways could be a new target for therapeutic and chemopreventive intervention. Metformin in particular is actually considered a promising agent against mitochondrial activity thanks to its ability to inhibit the mitochondrial complex I.

摘要

代谢重编程是指癌细胞改变其代谢的能力,以满足由于持续生长、快速增殖以及肿瘤细胞的其他典型特征而增加的能量需求。长期以来,人们一直认为代谢需求的增加与线粒体作用无关,但最近我们了解到,线粒体活性与代谢在调节肿瘤细胞生长和增殖所需能量方面起着关键作用。基于这些原因,线粒体途径可能成为治疗和化学预防干预的新靶点。特别是二甲双胍,由于其抑制线粒体复合物I的能力,实际上被认为是一种有前景的抗线粒体活性药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9689/4641168/4ee06e6e2552/BMRI2015-972193.001.jpg

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