Oliver's mTOR Atlas Evidence Platform
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mTOR regulates the pro-tumorigenic senescence-associated secretory phenotype by promoting IL1A translation

Laberge RM, Sun Y, Orjalo AV, Patil CK, Freund A, Campisi J · 2015 · Nature Cell Biology · Atlas ID LAB2015

What this study shows

Explained HOW rapamycin calms 'inflammaging'. Senescent cells spew inflammatory signals (the SASP) that damage surrounding tissue and even feed tumors. mTOR powers this by translating IL1A, the cytokine at the top of the cascade. Rapamycin selectively shuts it down - and blocked senescent cells from fueling prostate tumor growth in mice.

Abstract

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The TOR (target of rapamycin) kinase limits longevity by poorly understood mechanisms. Rapamycin suppresses the mammalian TORC1 complex, which regulates translation, and extends lifespan in diverse species, including mice. We show that rapamycin selectively blunts the pro-inflammatory phenotype of senescent cells. Cellular senescence suppresses cancer by preventing cell proliferation. However, as senescent cells accumulate with age, the senescence-associated secretory phenotype (SASP) can disrupt tissues and contribute to age-related pathologies, including cancer.

Read the full abstract on PubMed →

At a glance

Evidence type M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Human cells + mouse xenografts) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is.
Study type5 - Mechanistic / In Vitro
Model systemHuman cells + mouse xenografts
JournalNature Cell Biology
Year2015
Peer reviewedYes
Record last updated2026-08-22
SourceDOI 10.1038/ncb3195 · PMID 26147250 · Free full text (PMC4691706)

Extracted findings

InterventionRapamycin (mTORC1 inhibition)
TargetmTORC1 / IL1A / SASP
ModelHuman cells + mouse xenografts
EffectRapamycin blunts the pro-tumorigenic senescence-associated secretory phenotype by suppressing IL1A translation

In the Atlas

Related topics

RapamycinCellular senescencemTORC14E-BP1

Open questions that cite this study

More studies on this topic

Cite this paper

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Laberge, R. M., Sun, Y., Orjalo, A. V., Patil, C. K., Freund, A., & Campisi, J. (2015). mTOR regulates the pro-tumorigenic senescence-associated secretory phenotype by promoting IL1A translation. Nature Cell Biology. https://doi.org/10.1038/ncb3195

@article{LAB2015,
  author       = {Laberge, R. M. and Sun, Y. and Orjalo, A. V. and Patil, C. K. and Freund, A. and Campisi, J.},
  title        = {{mTOR regulates the pro-tumorigenic senescence-associated secretory phenotype by promoting IL1A translation}},
  journal      = {Nature Cell Biology},
  year         = {2015},
  doi          = {10.1038/ncb3195},
  note         = {PMID: 26147250},
}

Cite this Atlas record

The record is the Atlas's own work — the evidence label, the extracted findings and the links. It is cited as part of the dataset, not as the paper. 

Barton, O. (2026). Oliver's mTOR Atlas (record LAB2015) [Data set]. https://mtor-atlas.org/study/LAB2015/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_LAB2015,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record LAB2015},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/LAB2015/},
  doi          = {10.5281/zenodo.22059963}
}