ArticleMolecular and cellular biology1994
Cell transformation by c-fos requires an extended period of expression and is independent of the cell cycle.
Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 94 citations in OpenAlex.
- Truncated FOS impairs osteogenic differentiation and induces prostaglandin and NFκB signalling in an in vitro cell-of-origin model for osteoid osteoma and osteoblastoma.The Journal of pathology · 2026Article
- Transcriptomic Analysis Divulges Differential Expressions of Microglial Genes After Microglial Repopulation in Mice.International journal of molecular sciences · 2025Article
- CD38 promotes hematopoietic stem cell dormancy.PLoS biology · 2024Article
- Immediate Early Gene c-fos in the Brain: Focus on Glial Cells.Brain sciences · 2022Review
- JunB contributes to Id2 repression and the epithelial-mesenchymal transition in response to transforming growth factor-β.The Journal of cell biology · 2012Article
- c-Fos overexpression increases the proliferation of human hepatocytes by stabilizing nuclear Cyclin D1.World journal of gastroenterology · 2008Article
- Alternative splicing of c-fos pre-mRNA: contribution of the rates of synthesis and degradation to the copy number of each transcript isoform and detection of a truncated c-Fos immunoreactive species.BMC molecular biology · 2007Article
- Review
- Neuregulin 1-Beta cytoprotective role in AML 12 mouse hepatocytes exposed to pentachlorophenol.International journal of environmental research and public health · 2006Article
- AP-1 differentially expressed proteins Krp1 and fibronectin cooperatively enhance Rho-ROCK-independent mesenchymal invasion by altering the function, localization, and activity of nondifferentially expressed proteins.Molecular and cellular biology · 2006Article
- A-Raf and Raf-1 work together to influence transient ERK phosphorylation and Gl/S cell cycle progression.Oncogene · 2005Article
- Article
- A transcriptome map of cellular transformation by the fos oncogene.Molecular cancer · 2005Article
- An extracellular signal-regulated kinase 1- and 2-dependent program of chromatin trafficking of c-Fos and Fra-1 is required for cyclin D1 expression during cell cycle reentry.Molecular and cellular biology · 2004Article
- Article
- Invasion of normal human fibroblasts induced by v-Fos is independent of proliferation, immortalization, and the tumor suppressors p16INK4a and p53.Molecular and cellular biology · 2004Article
- Article
- The structural determinants responsible for c-Fos protein proteasomal degradation differ according to the conditions of expression.Oncogene · 2003Article
- Growth inhibition by the muscarinic M(3) acetylcholine receptor: evidence for p21(Cip1/Waf1) involvement in G(1) arrest.The Biochemical journal · 2002Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proto-oncogene transcription factors Fos and Jun form a heterodimeric complex that binds to DNA and regulates expression of specific target genes. Continuous expression of c-fos causes transformation of cultured fibroblasts and induces osteogenic sarcoma in mice. To investigate the molecular basis of fos-mediated oncogenesis, we developed a conditional cell transformation system in which Fos expression was regulated by isopropyl-beta-D-thiogalactopyranoside (IPTG). Synthesis or repression of Fos in L1-3c-fos cells occurred rapidly, within 30 min, after the removal or addition of IPTG to the culture medium. However, there was a significant delay between the induction of Fos expression and the appearance of morphological transformation. No effect was observed after 12 h of Fos expression, partial transformation was detected after 24 h, and full transformation required approximately 3 days of continuous Fos expression. Similarly, the transformed cell morphology persisted for at least 2 days after repression of Fos, and a normal phenotype was observed only after 3 days. Fos-Jun complexes, capable of binding to AP-1 sequences, were present continuously during the delay in morphological transformation. Furthermore, increased expression of several candidate Fos target genes, including those encoding Fra-1, transin (stromelysin), collagenase, and ornithine decarboxylase, was detected shortly after Fos induction. The induction of morphological transformation was not dependent on the cell cycle, as it occurred in both cycling and noncycling cells. Thus, the Fos-Jun complexes present before L1-3c-fos cells become fully transformed are transcriptionally active. These complexes disappeared, and the Fos target genes were repressed at least 2 days prior to reversion. Our results suggest that cell transformation by Fos requires increased expression of a target gene(s) with a long-lived product(s) that must reach a critical level.
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