ArticleAging2009
The relative contributions of the p53 and pRb pathways in oncogene-induced melanocyte senescence.
Article in Aging, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 74 citations in OpenAlex.
- Protein phosphatase 2A regulates senescence and immunogenicity in medulloblastoma models.The Journal of clinical investigation · 2026Article
- RPA hyperphosphorylation hinders the resolution of R-loops and G-quadruplex-associated R-loops during RAS-driven senescence.Nucleic acids research · 2026Article
- Senescence-associated and immune-related 9p21.3 locus genes in colorectal cancer: epigenetic architecture, molecular landscape and therapeutic possibilities.Frontiers in cell and developmental biology · 2026Review
- Unraveling senescence in cancer: mechanistic complexities and therapeutic opportunities.Molecular biology reports · 2025Review
- Senescent tumor cells in colorectal cancer are characterized by elevated enzymatic activity of complexes 1 and 2 in oxidative phosphorylation.Journal of pathology and translational medicine · 2023Article
- Potential of Telomerase in Age-Related Macular Degeneration-Involvement of Senescence, DNA Damage Response and Autophagy and a Key Role of PGC-1α.International journal of molecular sciences · 2021Review
- The effects of mutant Ras proteins on the cell signalome.Cancer metastasis reviews · 2020Review
- Senescence and Cancer: A Review of Clinical Implications of Senescence and Senotherapies.Cancers · 2020Review
- Article
- Jumonji C Demethylases in Cellular Senescence.Genes · 2019Review
- Interplay between small and long non-coding RNAs in cutaneous melanoma: a complex jigsaw puzzle with missing pieces.Molecular oncology · 2019Review
- Review
- Integration of ALV intoOncotarget · 2017Article
- The role of the NORE1A tumor suppressor in Oncogene-Induced Senescence.Cancer letters · 2017Review
- Both Complexity and Location of DNA Damage Contribute to Cellular Senescence Induced by Ionizing Radiation.PloS one · 2016Article
- Effective intra-S checkpoint responses to UVC in primary human melanocytes and melanoma cell lines.Pigment cell & melanoma research · 2016Article
- Disruptive chemicals, senescence and immortality.Carcinogenesis · 2015Review
- The Intricate Interplay between Mechanisms Underlying Aging and Cancer.Aging and disease · 2015Review
- Article
- Autophagy-independent senescence and genome instability driven by targeted telomere dysfunction.Autophagy · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncogene-induced senescence acts as a barrier against tumour formation and has been implicated as the mechanism preventing the transformation of benign melanocytic lesions that frequently harbour oncogenic B-RAF or N-RAS mutations. In the present study we systematically assessed the relative importance of the tumour suppressor proteins p53, p21(Waf1), pRb and p16(INK4a) in mediating oncogene-induced senescence in human melanocytes. We now show that oncogenic N-RAS induced senescence in melanocytes is associated with DNA damage, a potent DNA damage response and the activation of both the p16(INK4a)/pRb and p53/p21(Waf1) tumour suppressor pathways. Surprisingly neither the pharmacological inhibition of the DNA damage response pathway nor silencing of p53 expression had any detectable impact on oncogene-induced senescence in human melanocytes. Our data indicate that the pRb pathway is the dominant effector of senescence in these cells, as its specific inactivation delays the onset of senescence and weakens oncogene-induced proliferative arrest. Furthermore, we show that although both p16(INK4a) and p21(Waf1) are upregulated in response to N-RAS(Q61K), the activities of these CDK inhibitors are clearly distinct and only the loss of p16(INK4a) weakens senescence. We propose that the ability of p16(INK4a) to inhibit the cyclin D-dependent kinases and DNA replication, functions not shared by p21(Waf1), contribute to its role in senescence. Thus, in melanocytes with oncogenic signalling only p16(INK4a) can fully engage the pRb pathway to alter chromatin structure and silence the genes that are required for proliferation.
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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.