ArticleMolecular and cellular biology2004
Invasion of normal human fibroblasts induced by v-Fos is independent of proliferation, immortalization, and the tumor suppressors p16INK4a and p53.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 37 citations in OpenAlex.
- Compression-dependent microtubule reinforcement enables cells to navigate confined environments.Nature cell biology · 2024Article
- Tensin3 interaction with talin drives the formation of fibronectin-associated fibrillar adhesions.The Journal of cell biology · 2022Article
- Fibrogenic Lung Injury Induces Non-Cell-Autonomous Fibroblast Invasion.American journal of respiratory cell and molecular biology · 2016Article
- Annotation enrichment analysis: an alternative method for evaluating the functional properties of gene sets.Scientific reports · 2014Article
- Article
- Scar/WAVE3 contributes to motility and plasticity of lamellipodial dynamics but not invasion in three dimensions.The Biochemical journal · 2012Article
- The Arp2/3 activator WASH regulates α5β1-integrin-mediated invasive migration.Journal of cell science · 2011Article
- Identification of a structural motif in the tumor-suppressive protein GRIM-19 required for its antitumor activity.The American journal of pathology · 2010Article
- GRIM-19 inhibits v-Src-induced cell motility by interfering with cytoskeletal restructuring.Oncogene · 2009Article
- Chordoma and chondrosarcoma gene profile: implications for immunotherapy.Cancer immunology, immunotherapy : CII · 2009Article
- Profiling distinct mechanisms of tumour invasion for drug discovery: imaging adhesion, signalling and matrix turnover.Clinical & experimental metastasis · 2009Review
- p120-catenin is required for the collective invasion of squamous cell carcinoma cells via a phosphorylation-independent mechanism.Oncogene · 2007Article
- Review
- Calpain 2 and Src dependence distinguishes mesenchymal and amoeboid modes of tumour cell invasion: a link to integrin function.Oncogene · 2006Article
- p38gamma mitogen-activated protein kinase integrates signaling crosstalk between Ras and estrogen receptor to increase breast cancer invasion.Cancer research · 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
- RAS and TGF-beta exert antagonistic effects on extracellular matrix gene expression and fibroblast transformation.Oncogene · 2005Article
- Article
- Critical regulation of genes for tumor cell migration by AP-1.Clinical & experimental metastasis · 2004Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Invasion is generally perceived to be a late event during the progression of human cancer, but to date there are no consistent reports of alterations specifically associated with malignant conversion. We provide evidence that the v-Fos oncogene induces changes in gene expression that render noninvasive normal human diploid fibroblasts highly invasive, without inducing changes in growth factor requirements or anchorage dependence for proliferation. Furthermore, v-Fos-stimulated invasion is independent of the pRb/p16(INK4a) and p53 tumor suppressor pathways and telomerase. We have performed microarray analysis using Affymetrix GeneChips, and the gene expression profile of v-Fos transformed cells supports its role in the regulation of invasion, independent from proliferation. We also demonstrate that invasion, but not proliferation, is dependent on the activity of the up-regulated epidermal growth factor receptor. Taken together, these results indicate that AP-1-directed invasion could precede deregulated proliferation during tumorigenesis and that sustained activation of AP-1 could be the epigenetic event required for conversion of a benign tumor into a malignant one, thereby explaining why many malignant human tumors present without an obvious premalignant hyperproliferative dysplastic lesion.
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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.