ArticleOncogene2004
RUNX1 transformation of primary embryonic fibroblasts is revealed in the absence of p53.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 59 citations in OpenAlex.
- Targeting oncogene-induced senescence in ETV6::RUNX1 pre-leukemic cells.Cell death discovery · 2026Article
- Article
- Ginkgolide B increases healthspan and lifespan of female mice.Nature aging · 2025Article
- ARF alters PAF1 complex integrity to selectively repress oncogenic transcription programs upon p53 loss.Molecular cell · 2024Article
- Repression of developmental transcription factor networks triggers aging-associated gene expression in human glial progenitor cells.Nature communications · 2024Article
- Review
- Review
- The landscape of human tissue and cell type specific expression and co-regulation of senescence genes.Molecular neurodegeneration · 2022Article
- Oncogenic RUNX3: A Link between p53 Deficiency and MYC Dysregulation.Molecules and cells · 2020Review
- Role of RUNX Family Transcription Factors in DNA Damage Response.Molecules and cells · 2020Review
- Collaboration of MYC and RUNX2 in lymphoma simulates T-cell receptor signaling and attenuates p53 pathway activity.Journal of cellular biochemistry · 2019Article
- Profiling the epigenetic interplay of lncRNA RUNXOR and oncogenic RUNX1 in breast cancer cells by gene in situ cis-activation.American journal of cancer research · 2019Article
- 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
- LRG1 promotes proliferation and inhibits apoptosis in colorectal cancer cells via RUNX1 activation.PloS one · 2017Article
- Addiction to Runx1 is partially attenuated by loss of p53 in the Eµ-Myc lymphoma model.Oncotarget · 2016Article
- The RUNX family: developmental regulators in cancer.Nature reviews. Cancer · 2015Review
- Roles of AML1/RUNX1 in T-cell malignancy induced by loss of p53.Cancer science · 2013Article
- Response: the role of RUNX1 isoforms in hematopoietic commitment of human pluripotent stem cells.Blood · 2013Article
- The RUNX1 transcription factor is expressed in serous epithelial ovarian carcinoma and contributes to cell proliferation, migration and invasion.Cell cycle (Georgetown, Tex.) · 2013Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mammalian Runx gene family (Runx1-3) are transcription factors that play essential, lineage-specific roles in development. A growing body of evidence implicates these genes as mutational targets in cancer where, in different contexts, individual family members have been reported to act as tumour suppressors, dominant oncogenes or mediators of metastasis. We are exploring these paradoxical observations by ectopic expression of RUNX genes in primary murine embryonic fibroblasts where, in common with a number of other dominant oncogenes, RUNX1 induces senescence-like growth arrest in the presence of an intact p19(ARF)-p53 pathway. We now report that, in MEFs lacking functional p53, RUNX1 has apparently pro-oncogenic effects on cell growth that include cytoskeletal reorganization, reduced contact inhibition at confluence and accelerated tumour expansion in vivo. On the other hand, RUNX1 conferred no obvious growth advantage at low cell density and actually delayed entry of primary MEFs into S phase. We also found that ectopic RUNX1 interferes with the morphological and growth responses of p53-null MEFs to TGFbeta indicating that these effects are mediated by overlapping pathways. These observations help to elucidate the context-dependent consequences of loss and gain of Runx activity.
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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.