Targeting metabolism to influence cellular senescence a promising anti-cancer therapeutic strategy

被引:2
|
作者
Wang, Zehua [1 ,2 ]
Gao, Jianwen [3 ]
Xu, Congjian [1 ,2 ,4 ]
机构
[1] Fudan Univ, Obstet & Gynecol Hosp, Shanghai 200011, Peoples R China
[2] Shanghai Key Lab Female Reprod Endocrine Related D, Shanghai 200011, Peoples R China
[3] Shanghai Jian Qiao Univ, Coll Hlth Management, Shanghai 201306, Peoples R China
[4] Fudan Univ, Shanghai Med Sch, Dept Obstet & Gynecol, Shanghai 200032, Peoples R China
关键词
Senescence; Metabolic reprogramming; Senolytic; Aging; Anti -cancer treatment; CELLS; CANCER; MECHANISMS; HALLMARKS;
D O I
10.1016/j.biopha.2024.116962
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Metabolic disorders are considered the hallmarks of cancer and metabolic reprogramming is emerging as a new strategy for cancer treatment. Exogenous and endogenous stressors can induce cellular senescence; the interactions between cellular senescence and systemic metabolism are dynamic. Cellular senescence disrupts metabolic homeostasis in various tissues, which further promotes senescence, creating a vicious cycle facilitating tumor occurrence, recurrence, and altered outcomes of anticancer treatments. Therefore, the regulation of cellular senescence and related secretory phenotypes is considered a breakthrough in cancer therapy; moreover, proteins involved in the associated pathways are prospective therapeutic targets. Although studies on the association between cellular senescence and tumors have emerged in recent years, further elucidation of this complex correlation is required for comprehensive knowledge. In this paper, we review the research progress on the correlation between cell aging and metabolism, focusing on the strategies of targeting metabolism to modulate cellular senescence and the progress of relevant research in the context of anti-tumor therapy. Finally, we discuss the significance of improving the specificity and safety of anti-senescence drugs, which is a potential challenge in cancer therapy.
引用
收藏
页数:8
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