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Cellular senescence in tumor immune escape: Mechanisms, implications, and therapeutic potential

You, Li, Wu, Qinghua·2025·Critical Reviews in Oncology/Hematology
DOI 10.1016/j.critrevonc.2025.104628
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Abstract

Cellular senescence, a hallmark of aging, has emerged as a captivating area of research in tumor immunology with profound implications for cancer prevention and treatment. In the tumor microenvironment, senescent cells exhibit a dual role, simultaneously hindering tumor development through collaboration with immune cells and evading immune cell attacks by upregulating immunoinhibitory proteins. However, the intricate immune escape mechanism of cellular senescence in the tumor microenvironment remains a subject of intense investigation. Chronic inflammation is exacerbated by cellular senescence through the upregulation of pro-inflammatory factors such as interleukin-1β, thereby augmenting the risk of tumorigenesis. Additionally, the interplay between autophagy and cellular senescence adds another layer of complexity. Autophagy, known to slow down the aging process by reducing p53/p21 levels, may be downregulated by cellular senescence. To harness the therapeutic potential of cellular senescence, targeting its immunological aspects has gained significant attention. Strategies such as immune checkpoint inhibitors and T-cell senescence inhibition are being explored in the context of cellular senescence immunotherapy. In this comprehensive review, we provide a compelling overview of the regulation of cellular senescence and delve into the influencing factors, including chronic inflammation, autophagy, and circadian rhythms, associated with senescence in the tumor microenvironment.…

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Metadata

Authors
You, L., & Wu, Q.
Venue
Critical Reviews in Oncology/Hematology
Publisher
Elsevier BV
Published
2025-04
Volume
208
Pages
104628
ISSN
1040-8428
DOI
10.1016/j.critrevonc.2025.104628
Cited by
21
References
29
Language
en
Licence
Funders
National Natural Science Foundation of China (32373073, 31972741)

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