ArticleThe Journal of cell biology1993
Osteoblasts are target cells for transformation in c-fos transgenic mice.
Article in The Journal of cell biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
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Who cites it
103 citing papers in PubMed, 350 citations in OpenAlex.
- Sphingosine-1-Phosphate Promotes FOS Activation in Osteosarcoma Under Tumor Acidosis.Acta physiologica (Oxford, England) · 2026Article
- FOSL2 regulates endothelial cell state and chromatin accessibility in systemic sclerosis pulmonary vascular remodeling.JCI insight · 2026Article
- 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
- Fos-induced osteosarcoma growth causes a cachexia-like phenotype in mice and correlates with high Fgf21 serum levels.Cancer & metabolism · 2026Article
- FAPI TracerPharmaceuticals (Basel, Switzerland) · 2025Article
- Mouse Models of Osteosarcoma: Unraveling Disease Mechanisms and Accelerating Drug Discovery and Development.Cancer reports (Hoboken, N.J.) · 2025Review
- Rsk2 inhibition induces an aneuploid post-mitotic arrest of cell cycle progression in osteosarcoma cells.Cell death discovery · 2025Article
- The universal role of adaptive transcription in health and disease.The FEBS journal · 2025Review
- Integrated MicroRNA-mRNA Analyses of the Osteogenic Differentiation of Human Dental Pulp Stem Cells by a Helioxanthin Derivative.Current issues in molecular biology · 2024Article
- The RNA binding proteins LARP4A and LARP4B promote sarcoma and carcinoma growth and metastasis.iScience · 2024Article
- Metabolic rewiring controlled by c-Fos governs cartilage integrity in osteoarthritis.Annals of the rheumatic diseases · 2023Article
- Activator Protein-1 (AP-1) Signaling Inhibits the Growth of Ewing Sarcoma Cells in Response to DNA Replication Stress.Cancer research communications · 2023Article
- Genomic Redistribution of Metal-Response Transcription Factor-1 (MTF-1) in Cadmium Resistant Cells.Cells · 2023Article
- Improving Osteosarcoma Treatment: Comparative Oncology in Action.Life (Basel, Switzerland) · 2022Article
- Phylogenetic and Expression Analysis of Fos Transcription Factors in Zebrafish.International journal of molecular sciences · 2022Article
- Canine and murine models of osteosarcoma.Veterinary pathology · 2022Review
- Article
- The telomere complex and the origin of the cancer stem cell.Biomarker research · 2021Review
- Research models and mesenchymal/epithelial plasticity of osteosarcoma.Cell & bioscience · 2021Review
- BACH2-mediated FOS confers cytarabine resistance via stromal microenvironment alterations in pediatric ALL.Cancer science · 2021Observational
43 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have generated transgenic mice expressing the proto-oncogene c-fos from an H-2Kb class I MHC promoter as a tool to identify and isolate cell populations which are sensitive to altered levels of Fos protein. All homozygous H2-c-fosLTR mice develop osteosarcomas with a short latency period. This phenotype is specific for c-fos as transgenic mice expressing the fos- and jun-related genes, fosB and c-jun, from the same regulatory elements do not develop any pathology despite high expression in bone tissues. The c-fos transgene is not expressed during embryogenesis but is expressed after birth in bone tissues before the onset of tumor formation, specifically in putative preosteoblasts, bone-forming osteoblasts, osteocytes, as well as in osteoblastic cells present within the tumors. Primary and clonal cell lines established from c-fos-induced tumors expressed high levels of exogenous c-fos as well as the bone cell marker genes, type I collagen, alkaline phosphatase, and osteopontin/2ar. In contrast, osteocalcin/BGP expression was either low or absent. All cell lines were tumorigenic in vivo, some of which gave rise to osteosarcomas, expressing exogenous c-fos mRNA, and Fos protein in osteoblastic cells. Detailed analysis of one osteogenic cell line, P1, and several P1-derived clonal cell lines indicated that bone-forming osteoblastic cells were transformed by Fos. The regulation of osteocalcin/BGP and alkaline phosphatase gene expression by 1,25-dihydroxyvitamin D3 was abrogated in P1-derived clonal cells, whereas glucocorticoid responsiveness was unaltered. These results suggest that high levels of Fos perturb the normal growth control of osteoblastic cells and exert specific effects on the expression of the osteoblast phenotype.
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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.