The role of autophagy in regulating metabolism in the tumor microenvironment.
The role of autophagy in regulating metabolism in the tumor microenvironment.
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DOI：
10.1016/j.gendis.2021.10.010
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发表时间：
2023-03
期刊：
影响因子：
6.8
通讯作者：
Du, Yueyao
中科院分区：
文献类型：
--
作者：
Zhang, Panpan;Cheng, Shanshan;Sheng, Xiaonan;Dai, Huijuan;He, Kang;Du, Yueyao
自噬作为一种特殊的细胞程序性死亡，是消除细胞内异常蛋白或损伤细胞器以平衡细胞能量、促进细胞代谢的关键降解过程。自噬激活通过影响肿瘤微环境(TME)中间质细胞的代谢而日益被认为是肿瘤发生的重要标志。TME由肿瘤细胞、肿瘤相关成纤维细胞(CAF)、肿瘤相关内皮细胞(CAE)、免疫细胞和脂肪细胞组成。肿瘤细胞可以重复利用自噬参与的循环来维持线粒体的功能和能量供应，以满足其生长和增殖的代谢需求。然而，自噬可以促进肿瘤和间质细胞之间的串扰的机制尚不清楚。重编程代谢是TME的主要特征之一，导致肿瘤细胞具有不同机制的较高适应性。自噬的激活扩大了我们对肿瘤代谢与TME相互作用的理解。本文就自噬诱导的TME间质细胞与实体瘤细胞代谢串扰的最新研究进展作一综述，并揭示其潜在的治疗靶点。
Autophagy, as a special programmed cell death, is a critical degradative process that eliminates intracellular abnormal proteins or damage organelles to balance cell energy and favor cell metabolism with autophagy-related (ATG) proteins. Autophagy activation is being increasingly recognized as an essential hallmark in tumorigenesis through influencing the metabolism of stromal cells in the tumor microenvironment (TME) which comprises of tumor cells, cancer-associated fibroblasts (CAFs), cancer-associated endothelial cells (CAEs), immune cells and adipocytes. Tumor cells can reuse autophagy-involved recycling to maintain mitochondrial function and energy supply to meet the metabolic demand of their growth and proliferation. However, the mechanism through which autophagy can promote a crosstalk between tumor and stroma cells is not clear. Reprogramed metabolism is one of the main characteristics of TME leading to higher adaptability of tumor cells with diverse mechanisms. The activation of autophagy has expanded our understanding on the interaction between tumor metabolism and TME. The aim of this review is to report recent advances on the metabolic cross-talk between stromal cells and solid tumor cells induced by autophagy in TME and revealed potential therapeutic targets.
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影响因子：
5.9
作者：
Balaban S;Shearer RF;Lee LS;van Geldermalsen M;Schreuder M;Shtein HC;Cairns R;Thomas KC;Fazakerley DJ;Grewal T;Holst J;Saunders DN;Hoy AJ
通讯作者：
Hoy AJ
影响因子：
64.5
作者：
Cubillos-Ruiz JR;Silberman PC;Rutkowski MR;Chopra S;Perales-Puchalt A;Song M;Zhang S;Bettigole SE;Gupta D;Holcomb K;Ellenson LH;Caputo T;Lee AH;Conejo-Garcia JR;Glimcher LH
通讯作者：
Glimcher LH
DOI：
10.1186/s13058-016-0740-2
发表时间：
2016-08-11
期刊：
Breast cancer research : BCR
影响因子：
--
作者：
Bussard KM;Mutkus L;Stumpf K;Gomez-Manzano C;Marini FC
通讯作者：
Marini FC
氯喹通过将肿瘤相关巨噬细胞重置为 M1 表型来调节抗肿瘤免疫反应
影响因子：
16.6
作者：
Chen D;Xie J;Fiskesund R;Dong W;Liang X;Lv J;Jin X;Liu J;Mo S;Zhang T;Cheng F;Zhou Y;Zhang H;Tang K;Ma J;Liu Y;Huang B
通讯作者：
Huang B
影响因子：
64.5
作者：
De Bock, Katrien;Georgiadou, Maria;Carmeliet, Peter
通讯作者：
Carmeliet, Peter