Mitochondrial metabolism and cancer metastasis

被引:23
|
作者
Yu, Dandan [1 ,2 ,3 ]
Liu, Chang [1 ,2 ,4 ]
Guo, Ling [1 ,2 ]
机构
[1] Southern Univ Sci & Technol, Acad Adv Interdisciplinary Studies, Shenzhen Key Lab Cell Microenvironm, Guangdong Prov Key Lab Cell Microenvironm & Dis R, Shenzhen 518055, Peoples R China
[2] Southern Univ Sci & Technol, Dept Biol, Shenzhen 518055, Peoples R China
[3] Univ Hong Kong, Li Ka Shing Fac Med, Dept Clin Oncol, Hong Kong, Peoples R China
[4] Shenzhen Univ, Hlth Sci Ctr, Sch Basic Med Sci, Dept Anat Histol & Embryol, Shenzhen 518060, Peoples R China
关键词
Metastasis; mitochondrial metabolism; proline metabolism; extracellular matrix (ECM); tumor micro-environment (TME); MESENCHYMAL TRANSITION; GLUCOSE-METABOLISM; SUCCINATE-DEHYDROGENASE; FOCAL ADHESIONS; LACTATE SHUTTLE; MUTATIONS; INTEGRIN; HYPOXIA; FAMILY; GROWTH;
D O I
10.21037/atm.2020.03.42
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Metastasis is regarded as the most important cause of cancer-related deaths around the world. During the complicated metastatic cascade, altered mitochondrial metabolism adapts to serve distinct conditions and microenvironments. In this review, we discuss how cells regulate their mitochondria metabolism to adapt to environmental cues during the metastasis, as well as how cancer cells and their tumor micro-environment (TME) are metabolically coupled during the metastatic cascade. We place a strong emphasis on how mitochondrial proline metabolism and extracellular matrix (ECM) are coupled.
引用
收藏
页数:8
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