Phosphatidylcholine-Derived Lipid Mediators: The Crosstalk Between Cancer Cells and Immune Cells.
Phosphatidylcholine-Derived Lipid Mediators: The Crosstalk Between Cancer Cells and Immune Cells.
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DOI：
10.3389/fimmu.2022.768606
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发表时间：
2022
影响因子：
7.3
通讯作者：
Chammas R
中科院分区：
文献类型：
--
作者：
Saito RF;Andrade LNS;Bustos SO;Chammas R
为了产生耐药性，癌细胞需要激活和维持分子防御机制，该机制依赖于耐药性和基本功能之间的能量权衡。代谢重编程已被证明可以促进细胞生长并有助于癌症耐药性。最近，脂质代谢的变化已成为抗癌药物耐药性的重要驱动因素。在这篇综述中，我们强调了胆碱代谢的作用，重点关注磷脂酰胆碱循环在治疗抵抗调节中的作用。我们分析了磷脂酰胆碱及其代谢物对癌细胞细胞内过程的贡献，它们既是主要的细胞膜成分又是能量来源。我们进一步扩展了关于磷脂酰胆碱衍生的脂质介质在肿瘤微环境中癌症和免疫细胞之间的细胞通讯中的作用，以及它们在治疗失败的免疫调节中的关键作用的讨论。磷脂酰胆碱代谢的变化是响应应激条件而激活的适应性程序的一部分，该应激条件导致癌症治疗耐药性并为治疗耐药癌症提供了治疗机会。
To become resistant, cancer cells need to activate and maintain molecular defense mechanisms that depend on an energy trade-off between resistance and essential functions. Metabolic reprogramming has been shown to fuel cell growth and contribute to cancer drug resistance. Recently, changes in lipid metabolism have emerged as an important driver of resistance to anticancer agents. In this review, we highlight the role of choline metabolism with a focus on the phosphatidylcholine cycle in the regulation of resistance to therapy. We analyze the contribution of phosphatidylcholine and its metabolites to intracellular processes of cancer cells, both as the major cell membrane constituents and source of energy. We further extended our discussion about the role of phosphatidylcholine-derived lipid mediators in cellular communication between cancer and immune cells within the tumor microenvironment, as well as their pivotal role in the immune regulation of therapeutic failure. Changes in phosphatidylcholine metabolism are part of an adaptive program activated in response to stress conditions that contribute to cancer therapy resistance and open therapeutic opportunities for treating drug-resistant cancers.
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影响因子：
5.7
作者：
Beloueche-Babari, M;Jackson, LE;Ronen, SM
通讯作者：
Ronen, SM
影响因子：
11.2
作者：
Bae S;Ulrich CM;Neuhouser ML;Malysheva O;Bailey LB;Xiao L;Brown EC;Cushing-Haugen KL;Zheng Y;Cheng TY;Miller JW;Green R;Lane DS;Beresford SA;Caudill MA
通讯作者：
Caudill MA
影响因子：
11.2
作者：
Beloueche-Babari, M;Jackson, LE;Ronen, SM
通讯作者：
Ronen, SM
影响因子：
4.6
作者：
Bachi AL;Dos Santos LC;Nonogaki S;Jancar S;Jasiulionis MG
通讯作者：
Jasiulionis MG
DOI：
10.1093/jnci/djv371
发表时间：
2016-05
期刊：
Journal of the National Cancer Institute
影响因子：
--
作者：
Asim M;Massie CE;Orafidiya F;Pértega-Gomes N;Warren AY;Esmaeili M;Selth LA;Zecchini HI;Luko K;Qureshi A;Baridi A;Menon S;Madhu B;Escriu C;Lyons S;Vowler SL;Zecchini VR;Shaw G;Hessenkemper W;Russell R;Mohammed H;Stefanos N;Lynch AG;Grigorenko E;D'Santos C;Taylor C;Lamb A;Sriranjan R;Yang J;Stark R;Dehm SM;Rennie PS;Carroll JS;Griffiths JR;Tavaré S;Mills IG;McEwan IJ;Baniahmad A;Tilley WD;Neal DE
通讯作者：
Neal DE