ArticleMolecular and cellular biology2004
Normal human fibroblasts are resistant to RAS-induced senescence.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
52 citing papers in PubMed, 106 citations in OpenAlex.
- TAD boundaries and gene activity are uncoupled.eLife · 2026Article
- TAD boundaries and gene activity are uncoupled.bioRxiv : the preprint server for biology · 2026Article
- The complex journey of targeting RAS in oncology.BMC cancer · 2025Review
- Cell type- and transcription-independent spatial proximity between enhancers and promoters.Molecular biology of the cell · 2024Article
- Allele-level visualization of transcription and chromatin by high-throughput imaging.Histochemistry and cell biology · 2024Article
- Allele-level visualization of transcription and chromatin by high-throughput imaging.Research square · 2024Article
- Allele-level visualization of transcription and chromatin by high-throughput imaging.bioRxiv : the preprint server for biology · 2024Article
- Mechanisms and Regulation of Cellular Senescence.International journal of molecular sciences · 2021Review
- Possibility of inducing tumor cell senescence during therapy.Oncology letters · 2021Review
- DNAJB9 Inhibits p53-Dependent Oncogene-Induced Senescence and Induces Cell Transformation.Molecules and cells · 2020Article
- The coordinate actions of calcineurin and Hog1 mediate the stress response through multiple nodes of the cell cycle network.PLoS genetics · 2020Article
- Article
- High-efficiency RNA-based reprogramming of human primary fibroblasts.Nature communications · 2018Article
- MYC and RAS are unable to cooperate in overcoming cellular senescence and apoptosis in normal human fibroblasts.Cell cycle (Georgetown, Tex.) · 2018Article
- Uncoupling Oncogene-Induced Senescence (OIS) and DNA Damage Response (DDR) triggered by DNA hyper-replication: lessons from primary mouse embryo astrocytes (MEA).Scientific reports · 2017Article
- Ki-67 Contributes to Normal Cell Cycle Progression and Inactive X Heterochromatin in p21 Checkpoint-Proficient Human Cells.Molecular and cellular biology · 2017Article
- Comparative analysis of 2D and 3D distance measurements to study spatial genome organization.Methods (San Diego, Calif.) · 2017Article
- The Immortal Senescence.Methods in molecular biology (Clifton, N.J.) · 2017Review
- A separable domain of the p150 subunit of human chromatin assembly factor-1 promotes protein and chromosome associations with nucleoli.Molecular biology of the cell · 2014Article
- Spread of X-chromosome inactivation into autosomal sequences: role for DNA elements, chromatin features and chromosomal domains.Human molecular genetics · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
Oncogenic stimuli are thought to induce senescence in normal cells in order to protect against transformation and to induce proliferation in cells with altered p53 and/or retinoblastoma (Rb) pathways. In human fibroblasts, RAS initiates senescence through upregulation of the cyclin-dependent kinase inhibitor p16INK4A. We show here that in contrast to cultured fibroblast strains, freshly isolated normal fibroblasts are resistant to RAS-induced senescence and instead show some characteristics of transformation. RAS did not induce growth arrest or expression of senescence-associated beta-galactosidase, and Rb remained hyperphosphorylated despite elevated levels of p16. Instead, RAS promoted anchorage-independent growth of normal fibroblasts, although expression of hTert with RAS increased colony formation and allowed normal fibroblasts to bypass contact inhibition. To test the hypothesis that p16 levels determine how cells respond to RAS, we expressed RAS in freshly isolated fibroblasts that expressed very low levels of p16, in hTert-immortalized fibroblasts that had accumulated intermediate levels of p16, and in IMR90 fibroblasts with high levels of p16. RAS induced growth arrest in cells with higher p16 levels, and this effect was reversed by p16 knockdown in the hTert-immortalized fibroblasts. These findings indicate that culture-imposed stress sensitizes cells to RAS-induced arrest, whereas early passage cells do not arrest in response to RAS.
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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.