Metabolic reprogramming: a bridge between aging and tumorigenesis.
Metabolic reprogramming: a bridge between aging and tumorigenesis.
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代谢重编程:衰老与肿瘤发生之间的桥梁。
DOI:
10.1002/1878-0261.13261
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发表时间:
2022-09
影响因子:
6.6
通讯作者:
Gomes, Ana P.
中科院分区:
文献类型:
--
作者:
Drapela, Stanislav;Ilter, Didem;Gomes, Ana P.
Aging is the most robust risk factor for cancer development, with more than 60% of cancers occurring in those aged 60 and above. However, how aging and tumorigenesis are intertwined is poorly understood and a matter of significant debate. Metabolic changes are hallmarks of both aging and tumorigenesis. The deleterious consequences of aging include dysfunctional cellular processes, the build‐up of metabolic byproducts and waste molecules in circulation and within tissues, and stiffer connective tissues that impede blood flow and oxygenation. Collectively, these age‐driven changes lead to metabolic reprogramming in different cell types of a given tissue that significantly affects their cellular functions. Here, we put forward the idea that metabolic changes that happen during aging help create a favorable environment for tumorigenesis. We review parallels in metabolic changes that happen during aging and how these changes function both as adaptive mechanisms that enable the development of malignant phenotypes in a cell‐autonomous manner and as mechanisms that suppress immune surveillance, collectively creating the perfect environment for cancers to thrive. Hence, antiaging therapeutic strategies that target the metabolic reprogramming that occurs as we age might provide new opportunities to prevent cancer initiation and/or improve responses to standard‐of‐care anticancer therapies. Tumorigenicity and immune function are linked to the metabolic status of the host. As an organism ages, changes in metabolism, including changes in nutrient sensing, cellular energetics, and redox balance, produce an environment conducive to tumor initiation. Thus, strategies that promote metabolic rejuvenation might prevent age‐related tumor initiation and enhance the effectiveness of anticancer therapies.
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影响因子:
8.8
作者:
Brown K;Xie S;Qiu X;Mohrin M;Shin J;Liu Y;Zhang D;Scadden DT;Chen D
通讯作者:
Chen D
DOI:
10.1016/0921-8734(92)90020-p
发表时间:
1992-09-01
期刊:
MUTATION RESEARCH
影响因子:
--
作者:
ARNHEIM, N;CORTOPASSI, G
通讯作者:
CORTOPASSI, G
影响因子:
29
作者:
Chatterjee S;Daenthanasanmak A;Chakraborty P;Wyatt MW;Dhar P;Selvam SP;Fu J;Zhang J;Nguyen H;Kang I;Toth K;Al-Homrani M;Husain M;Beeson G;Ball L;Helke K;Husain S;Garrett-Mayer E;Hardiman G;Mehrotra M;Nishimura MI;Beeson CC;Bupp MG;Wu J;Ogretmen B;Paulos CM;Rathmell J;Yu XZ;Mehrotra S
通讯作者:
Mehrotra S
影响因子:
3.9
作者:
CEDERGREN, R;GRAY, MW;SANKOFF, D
通讯作者:
SANKOFF, D
影响因子:
29
作者:
Bjedov I;Toivonen JM;Kerr F;Slack C;Jacobson J;Foley A;Partridge L
通讯作者:
Partridge L