The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
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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“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]
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In the citing paper
“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]
Experimental — accuracy not yet measuredIn the citing paper
“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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Cites
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“This up-regulation of inflammatory factors during aging could be the cause of the senescence-associated secretory phenotype, which causes a secretion of inflammatory factors to the surrounding environment leading to bystander senescence of nearby cells or even transformation of nearby pre-malignant cells.(30) However,…”
BackgroundThe essence of senescence: Figure 1.
Kuilman, T., Michaloglou, C., Mooi, W. J., & Peeper, D. S. (2010) · Genes & Development · doi:10.1101/gad.1971610 · Cited by 2,038
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Metadata
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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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