ArticleOncogene2003
The proto-oncoprotein c-Fos negatively regulates hepatocellular tumorigenesis.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 79 citations in OpenAlex.
- Germacrone suppresses renal cancer growth by regulating c-Fos-mediated lipid metabolism.Lipids in health and disease · 2026Article
- Direct aldosterone stimulation of skeletal muscle fibroblasts changes gene expression and differentially affects fibroblast functions from normal and diseased muscles.Frontiers in physiology · 2026Article
- C-FOS inhibition promotes pancreatic cancer cell ferroptosis by transcriptionally regulating the expression of SLC7A11.Functional & integrative genomics · 2024Article
- Combinatorial Treatment with PARP-1 Inhibitors and Cisplatin Attenuates Cervical Cancer Growth through Fos-Driven Changes in Gene Expression.Molecular cancer research : MCR · 2022Article
- Revealing nuclear receptor hub modules from Basal-like breast cancer expression networks.PloS one · 2021Article
- The Adipokine Component in the Molecular Regulation of Cancer Cell Survival, Proliferation and Metastasis.Pathology oncology research : POR · 2021Review
- Article
- Chemerin and Cancer.International journal of molecular sciences · 2019Review
- NFBTA: A Potent Cytotoxic Agent against Glioblastoma.Molecules (Basel, Switzerland) · 2019Article
- Identification of Key Genes and Pathways in Cervical Cancer by Bioinformatics Analysis.International journal of medical sciences · 2019Article
- Overexpression of aryl hydrocarbon receptor (AHR) signalling pathway in human meningioma.Journal of neuro-oncology · 2018Article
- Evidence for Homodimerization of the c-Fos Transcription Factor in Live Cells Revealed by Fluorescence Microscopy and Computer Modeling.Molecular and cellular biology · 2015Article
- Up-regulation of c-Fos associated with neuronal apoptosis following intracerebral hemorrhage.Cellular and molecular neurobiology · 2015Article
- Targeting HOX transcription factors in prostate cancer.BMC urology · 2014Article
- c-FOS suppresses ovarian cancer progression by changing adhesion.British journal of cancer · 2014Article
- Identifying gastric cancer related genes using the shortest path algorithm and protein-protein interaction network.BioMed research international · 2014Article
- Article
- Liver cancer initiation is controlled by AP-1 through SIRT6-dependent inhibition of survivin.Nature cell biology · 2012Article
- Emerging roles of ATF2 and the dynamic AP1 network in cancer.Nature reviews. Cancer · 2010Review
- Epithelial-mesenchymal transition in hepatocellular carcinoma.Future oncology (London, England) · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocytes adopt an invasive and metastatic phenotype caused by the cooperation of transforming growth factor (TGF)-beta and oncogenic Ha-Ras. In the initial phase of this process, c-Fos is rapidly induced by TGF-beta, but then decreases to undetectable levels. Here, we investigated the functional implications of c-Fos activation and its contribution to hepatocellular tumorigenesis. By employing conditional c-Fos expression, we observed that continuous activation of c-Fos and consequently AP-1 activity leads to depolarization of differentiated murine epithelial hepatocytes. Most remarkably, this change in morphology was associated with inhibition of proliferation and induction of cell death. Coexpression of antiapoptotic Bcl-XL or scavenging of reactive oxygen species was sufficient to prevent the c-Fos-mediated phenotype. In contrast, the cooperation of c-Fos with oncogenic Ha-Ras or a Ras mutant selectively activating the MAPK pathway even enhanced c-Fos-induced effects. Showing the negative role in hepatocellular tumorigenesis, c-Fos repressed oncogenic Ras-driven anchorage-independent growth in vitro and strongly suppressed tumour formation in vivo. Taken together, we demonstrate that c-Fos modulates plasticity of epithelial hepatocytes and acts tumour suppressive in neoplastic hepatocytes by stimulating cell cycle inhibition and cell death.
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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.