ArticleCancer research2007
Runx2 disruption promotes immortalization and confers resistance to oncogene-induced senescence in primary murine fibroblasts.
Article in Cancer research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
The trial behind it
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
34 citing papers in PubMed, 52 citations in OpenAlex.
- Targeting oncogene-induced senescence in ETV6::RUNX1 pre-leukemic cells.Cell death discovery · 2026Article
- Extracellular vesicles from long COVID patients promote RUNX2-mediated cellular stress via dysregulated miR-204 and p53 pathway activation.Cell communication and signaling : CCS · 2025Article
- Impaired MC3T3-E1 osteoblast differentiation triggered by oncogenic HRAS is rescued by the farnesyltransferase inhibitor Tipifarnib.Scientific reports · 2025Article
- Repression of developmental transcription factor networks triggers aging-associated gene expression in human glial progenitor cells.Nature communications · 2024Article
- Review
- Article
- Article
- The Role of Chondrocyte Hypertrophy and Senescence in Osteoarthritis Initiation and Progression.International journal of molecular sciences · 2020Review
- Collaboration of MYC and RUNX2 in lymphoma simulates T-cell receptor signaling and attenuates p53 pathway activity.Journal of cellular biochemistry · 2019Article
- RUNX family: Oncogenes or tumor suppressors (Review).Oncology reports · 2019Review
- Functional relationship between p53 and RUNX proteins.Journal of molecular cell biology · 2019Review
- RUNX-mediated growth arrest and senescence are attenuated by diverse mechanisms in cells expressing RUNX1 fusion oncoproteins.Journal of cellular biochemistry · 2018Article
- Runx1 Orchestrates Sphingolipid Metabolism and Glucocorticoid Resistance in Lymphomagenesis.Journal of cellular biochemistry · 2017Article
- Frequent infection of human cancer xenografts with murine endogenous retroviruses in vivo.Viruses · 2015Article
- The RUNX family: developmental regulators in cancer.Nature reviews. Cancer · 2015Review
- RUNX2 correlates with subtype-specific breast cancer in a human tissue microarray, and ectopic expression of Runx2 perturbs differentiation in the mouse mammary gland.Disease models & mechanisms · 2014Article
- The cancer-related transcription factor Runx2 modulates cell proliferation in human osteosarcoma cell lines.Journal of cellular physiology · 2013Article
- MuMoD: a Bayesian approach to detect multiple modes of protein-DNA binding from genome-wide ChIP data.Nucleic acids research · 2013Article
- Loss of RASSF1A synergizes with deregulated RUNX2 signaling in tumorigenesis.Cancer research · 2012Article
- Runx2 controls a feed-forward loop between androgen and prolactin-induced protein (PIP) in stimulating T47D cell proliferation.Journal of cellular physiology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The Runx genes play paradoxical roles in cancer where they can function either as dominant oncogenes or tumor suppressors according to context. We now show that the ability to induce premature senescence in primary murine embryonic fibroblasts (MEF) is a common feature of all three Runx genes. However, ectopic Runx-induced senescence contrasts with Ras oncogene-induced senescence, as it occurs directly and lacks the hallmarks of proliferative stress. Moreover, a fundamental role for Runx function in the senescence program is indicated by the effects of Runx2 disruption, which renders MEFs prone to spontaneous immortalization and confers an early growth advantage that is resistant to stress-induced growth arrest. Runx2(-/-) cells are refractory to H-Ras(V12)-induced premature senescence, despite the activation of a cascade of growth inhibitors and senescence markers, and are permissive for oncogenic transformation. The aberrant behavior of Runx2(-/-) cells is associated with signaling defects and elevated expression of S-G(2)-M cyclins and their associated cyclin dependent kinase activities that may override the effects of growth inhibitory signals. Coupling of stress responses to the cell cycle represents a novel facet of Runx tumor suppressor function and provides a rationale for the lineage-specific effects of loss of Runx function in cancer.
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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.