Gene expression profiling of replicative and induced senescence
Open accessAbstract
Cellular senescence is a cell cycle arrest accompanied by high expression of cyclin dependent kinase inhibitors which counteract overactive growth signals, which serves as a tumor suppressive mechanism. Senescence can be a result of telomere shortening (natural or replicative senescence) or DNA damage resulting from exogenous stressors (induced senescence). Here, we performed gene expression profiling through RNA-seq of replicative senescence, adriamycin-induced senescence, H2O2-induced senescence, and 5-aza-2-deoxycytidine-induced senescence in order to profile the pathways controlling various types of senescence. Overall, the pathways common to all 4 types of senescence were related to inflammation and the innate immune system. It was also evident that 5-aza-induced senescence mirrors natural replicative senescence due to telomere shortening. We also examined the prevalence of senescence-associated secretory phenotype (SASP) factors in the RNA-seq data, showing that it is a common characteristic of all 4 types of senescence. In addition, we could discriminate changes in gene expression due to quiescence during cellular senescence from those that were specific to senescence.
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SenMayo performed better than six existing senescence/SASP gene panels.
“Using publicly available RNA-seq data, we demonstrated applicability across tissues and species and also found that SenMayo performed better than six existing senescence/SASP gene panels14,42–46.”
From A new gene set identifies senescent cells and predicts senescence-associated pathways across tissues (2022) · cites this paper as [43]
SenMayo consistently outperformed six additional senescence/SASP gene sets in identifying senescent cells with aging across tissues and species and in demonstrating responses to senescent cell clearance.
“SenMayo consistently outperformed these gene sets (based on normalized enrichment scores [NES] and p values) both in the ability to identify senescent cells with aging across tissues and species and in demonstrating responses to senescent cell clearance.”
From A new gene set identifies senescent cells and predicts senescence-associated pathways across tissues (2022) · cites this paper as [43]
The Results section identifies genes shared across four types of senescence, and the Discussion describes SASP expression across those types. Searches for SenMayo, comparisons with six gene sets, normalized enrichment scores, and responses to senescent-cell clearance found no passage addressing the claimed performance comparison. The available passages have no page numbers. (LLM, conf=0.76)
Experimental — accuracy not yet measuredCell-cycle arrest, changes in gene expression and phenotypic changes that accompany cellular senescence constitute serious restrictions in the functionality of different cell types.
“However, cell-cycle arrest, changes in gene expression and phenotypic changes that accompany cellular senescence constitute serious restrictions in the functionality of different cell types [119].”
From Ageing, Cellular Senescence and Neurodegenerative Disease (2018) · cites this paper as [119]
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- Authors
- Purcell, M., Kruger, A., & Tainsky, M. A.
- Affiliations
- Wayne State University (US)
- Applied Genomics Technology Center at Wayne State University
- Corresponding author
- Tainsky, Michael A
- ORCID
- Tainsky, Michael A
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2014-12-15
- Volume
- 13
- Issue
- 24
- Pages
- 3927-3937
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- PMC
- PMC4615143
- OpenAlex
- W2127506701
- Cited by
- 132
- References
- 41
- Citations by year
- 2026: 15 · 2025: 17 · 2024: 14 · 2023: 9 · 2022: 9 · 2021: 13 · 2020: 13 · 2019: 11 · 2018: 13 · 2017: 7 · 2016: 8 · 2015: 3
- FWCI
- 3.99
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wayne State University (P30 CA 022453)
- Barbara Ann Karmanos Cancer Institute (P30 CA022453)
- National Cancer Institute (P30CA022453)
- 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 › Single-cell and spatial transcriptomics
- Keywords
- cellular senescence, replicative senescence, induced senescence, telomere shortening, hydrogen peroxide-induced senescence, senescence-associated secretory phenotype, inflammation, innate immune system, quiescence, gene expression profiling, cyclin-dependent kinase inhibitors
- MeSH terms
- Decitabine, Azacitidine, Doxorubicin, Humans, Hydrogen Peroxide, Interleukin-1, Gene Expression, Cellular Senescence, Sequence Analysis, RNA, Gene Expression Profiling, Cell Line, Tumor, Cyclin A2
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