Mitochondrial metabolism-mediated redox regulation in cancer progression.

Mitochondrial metabolism-mediated redox regulation in cancer progression.
复制标题

癌症进展中线粒体代谢介导的氧化还原调节。

DOI:
10.1016/j.redox.2021.101870
复制
发表时间:
2021-06
期刊:
影响因子:
11.4
通讯作者:
Kang S
Kang S
中科院分区:
生物学1区
文献类型:
--
作者:
Boese AC;Kang S

文献摘要

参考文献

被引文献

相似文献

癌细胞由于癌基因的激活和肿瘤抑制基因的丢失而显示出异常的代谢活性。瓦尔堡效应是癌症的常见代谢特征,其涉及有氧糖酵解优于氧化磷酸化以产生ATP和生物合成的构件。然而,新出现的证据表明,线粒体代谢途径也在癌症中重新编程,并在生物能量学,生物合成和管理氧化还原稳态中发挥重要作用。线粒体作为代谢途径的中心枢纽,产生ATP和脂质、核酸和蛋白质生物合成的结构单元。然而,线粒体呼吸也是活性氧的主要来源,如果水平过高,活性氧会破坏细胞器并引发细胞死亡。一般来说,据报道癌细胞比其非癌细胞具有更高水平的活性氧,因此必须采用不同的代谢策略来防止氧化应激。然而,越来越多的证据表明,增殖和扩散的癌细胞之间的代谢谱是不一样的。在这篇综述中,我们将研究线粒体代谢途径,如氨解,增殖和扩散的癌细胞利用控制其氧化还原状态。
Cancer cells display abnormal metabolic activity as a result of activated oncogenes and loss of tumor suppressor genes. The Warburg Effect is a common metabolic feature of cancer that involves a preference for aerobic glycolysis over oxidative phosphorylation to generate ATP and building blocks for biosynthesis. However, emerging evidence indicates that mitochondrial metabolic pathways are also reprogrammed in cancer and play vital roles in bioenergetics, biosynthesis, and managing redox homeostasis. The mitochondria act a central hub for metabolic pathways that generate ATP and building blocks for lipid, nucleic acid and protein biosynthesis. However, mitochondrial respiration is also a leading source of reactive oxygen species that can damage cellular organelles and trigger cell death if levels become too high. In general, cancer cells are reported to have higher levels of reactive oxygen species than their non-cancerous cells of origin, and therefore must employ diverse metabolic strategies to prevent oxidative stress. However, mounting evidence indicates that the metabolic profiles between proliferative and disseminated cancer cells are not the same. In this review, we will examine mitochondrial metabolic pathways, such as glutaminolysis, that proliferative and disseminated cancer cells utilize to control their redox status.
DOI: 10.1038/cddis.2011.96
发表时间: 2011-10-06
影响因子: 9
作者:
通讯作者: --
DOI: 10.1126/science.1211485
发表时间: 2011-12-02
期刊: Science (New York, N.Y.)
影响因子: --
作者:
Anastasiou D;Poulogiannis G;Asara JM;Boxer MB;Jiang JK;Shen M;Bellinger G;Sasaki AT;Locasale JW;Auld DS;Thomas CJ;Vander Heiden MG;Cantley LC
通讯作者: Cantley LC
DOI: 10.1016/j.molcel.2012.12.026
发表时间: 2013-02-07
期刊: MOLECULAR CELL
影响因子: 16
作者:
Andersen, Joshua L.;Kornbluth, Sally
通讯作者: Kornbluth, Sally
DOI: 10.1126/science.aaw9872
发表时间: 2020-04-03
期刊: Science (New York, N.Y.)
影响因子: --
作者:
Badgley MA;Kremer DM;Maurer HC;DelGiorno KE;Lee HJ;Purohit V;Sagalovskiy IR;Ma A;Kapilian J;Firl CEM;Decker AR;Sastra SA;Palermo CF;Andrade LR;Sajjakulnukit P;Zhang L;Tolstyka ZP;Hirschhorn T;Lamb C;Liu T;Gu W;Seeley ES;Stone E;Georgiou G;Manor U;Iuga A;Wahl GM;Stockwell BR;Lyssiotis CA;Olive KP
通讯作者: Olive KP
DOI: 10.1038/nature17393
发表时间: 2016-04-14
期刊: Nature
影响因子: 64.8
作者:
Jiang L;Shestov AA;Swain P;Yang C;Parker SJ;Wang QA;Terada LS;Adams ND;McCabe MT;Pietrak B;Schmidt S;Metallo CM;Dranka BP;Schwartz B;DeBerardinis RJ
通讯作者: DeBerardinis RJ