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Lung cancer

Senescent macrophages drive lung cancer and accumulate in aging

Nature Aging volume 3, page 757 (2023)Cite this article

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“Previously, we have observed that removing naturally occurring p16Ink4a-positive senescent cells with the INK-ATTAC transgene delays tumor onset in old mice, but the mechanistic underpinning for how senescent cells contribute to tumor formation remained unclear”, explains Darren Baker. To explore the induction and consequences of senescence in tumorigenesis, both teams used mouse models of oncogenic KRAS-driven lung cancer, which form progressive lung lesions over a short time frame.

Baker’s team carefully profiled developing lung lesions and noted an upregulation of senescence markers within the lesions, which was particularly apparent in the early (hyperplasia) phase. The other team used an alternative strategy: “We devised a novel mouse model, known as p16-FDR, which enabled us to visualize, isolate, genetically trace, and selectively eliminate p16-expressing cell populations”, says Scott Haston. Both groups additionally used single-cell RNA sequencing and histological validation, and collectively identified a subpopulation of macrophages that expressed p16 and a selection of senescence-associated secretory phenotype (SASP) factors, which were sensitive to genetic (INK-ATTAC and p16-FDR) and pharmacological (ABT-263 and ABT-737) senolysis.

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  1. Nature Aging https://www.nature.com/nataging/

    Hannah Walters

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  1. Hannah Walters
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Correspondence to Hannah Walters.

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Walters, H. Senescent macrophages drive lung cancer and accumulate in aging. Nat Aging 3, 757 (2023). https://doi.org/10.1038/s43587-023-00459-1

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