NF90 coordinately represses the senescence-associated secretory phenotype
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A hallmark trait of cellular senescence is the acquisition of a senescence-associated secretory phenotype (SASP). SASP factors include cytokines and their receptors (IL-6, IL-8, osteoprotegerin, GM-CSF), chemokines and their ligands (MCP-1, HCC4), and oncogenes (Gro1 and Gro2), many of them encoded by mRNAs whose stability and translation are tightly regulated. Using two models of human fibroblast senescence (WI-38 and IDH4 cells), we report the identification of RNA-binding protein NF90 as a post-transcriptional repressor of several SASP factors. In 'young', proliferating fibroblasts, NF90 was highly abundant, associated with numerous SASP mRNAs, and inhibited their expression. By contrast, senescent cells expressed low levels of NF90, thus allowing SASP factor expression to increase. NF90 elicited these effects mainly by repressing the translation of target SASP mRNAs, since silencing NF90 did not increase the steady-state levels of SASP mRNAs but elevated key SASP factors including MCP-1, GROa, IL-6, and IL-8. Our findings indicate that NF90 contributes to maintaining low levels of SASP factors in non-senescent cells, while NF90 reduction in senescent cells allows SASP factor expression to rise.
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Senescent cells express reduced levels of NF90, an RNA-binding protein that suppresses translation of SASP factors such as MCP1, GROα, and IL-6.
“Senescent cells express reduced levels of nuclear factor (NF90), an RNA-binding protein that suppresses the translation of SASP factors, such as MCP1, GROα, and IL-6 [186].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [186]
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Self-citation
- Authors
- Tominaga-Yamanaka, K., Abdelmohsen, K., Martindale, J. L., Yang, X., Taub, D. D., & Gorospe, M.
- Affiliations
- Laboratory of Genetics, National Institute on Aging-Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA
- National Institutes of Health (US)
- Corresponding author
- Gorospe, Myriam
- Venue
- Aging
- Publisher
- Impact Journals, LLC
- Published
- 2012-10-31
- Volume
- 4
- Issue
- 10
- Pages
- 695-708
- ISSN
- 1945-4589 (ISSN-L)
- PMC
- PMC3517940
- OpenAlex
- W2124887931
- Cited by
- 49
- References
- 50
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 1 · 2023: 4 · 2022: 4 · 2021: 5 · 2020: 3 · 2019: 3 · 2018: 4 · 2017: 3 · 2016: 3 · 2015: 4 · 2014: 2 · 2013: 6 · 2012: 1
- FWCI
- 2.79
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- Aging (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
- Keywords
- NF90, senescence-associated secretory phenotype, cellular senescence, RNA-binding proteins, post-transcriptional regulation, translation repression, fibroblast senescence, MCP-1, interleukin-6, interleukin-8, chemokines, cytokines, mRNA stability
- MeSH terms
- Aging, Animals, Cell Line, Fibroblasts, Humans, Phenotype, RNA, Messenger, Interleukin-6, Interleukin-8, Cellular Senescence, Chemokine CCL2, Nuclear Factor 90 Proteins, Chemokine CXCL1
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