ArticleJournal of aging research2011
Self-Renewal Signalling in Presenescent Tetraploid IMR90 Cells.
Article in Journal of aging research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Review
- Review
- DNA damage invokes mitophagy through a pathway involving Spata18.Nucleic acids research · 2020Article
- Disentangling the aneuploidy and senescence paradoxes: a study of triploid breast cancers non-responsive to neoadjuvant therapy.Histochemistry and cell biology · 2016Article
- Article
- Role of stress-activated OCT4A in the cell fate decisions of embryonal carcinoma cells treated with etoposide.Cell cycle (Georgetown, Tex.) · 2015Article
- De-regulated expression of the BRG1 chromatin remodeling factor in bone marrow mesenchymal stromal cells induces senescence associated with the silencing of NANOG and changes in the levels of chromatin proteins.Cell cycle (Georgetown, Tex.) · 2015Article
- The "virgin birth", polyploidy, and the origin of cancer.Oncoscience · 2015Review
- Three steps to the immortality of cancer cells: senescence, polyploidy and self-renewal.Cancer cell international · 2013Article
- Low-dose etoposide-treatment induces endoreplication and cell death accompanied by cytoskeletal alterations in A549 cells: Does the response involve senescence? The possible role of vimentin.Cancer cell international · 2013Article
- DNA damage causes TP53-dependent coupling of self-renewal and senescence pathways in embryonal carcinoma cells.Cell cycle (Georgetown, Tex.) · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endopolyploidy and genomic instability are shared features of both stress-induced cellular senescence and malignant growth. Here, we examined these facets in the widely used normal human fibroblast model of senescence, IMR90. At the presenescence stage, a small (2-7%) proportion of cells overcome the 4n-G1 checkpoint, simultaneously inducing self-renewal (NANOG-positivity), the DNA damage response (DDR; γ-H2AX-positive foci), and senescence (p16inka4a- and p21CIP1-positivity) signalling, some cells reach octoploid DNA content and divide. All of these markers initially appear and partially colocalise in the perinucleolar compartment. Further, with development of senescence and accumulation of p16inka4a and p21CIP1, NANOG is downregulated in most cells. The cells increasingly arrest in the 4n-G1 fraction, completely halt divisions and ultimately degenerate. A positive link between DDR, self-renewal, and senescence signalling is initiated in the cells overcoming the tetraploidy barrier, indicating that cellular and molecular context of induced tetraploidy during this period of presenescence is favourable for carcinogenesis.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.