ArticleMolecular and cellular biology1996
Constitutive activation of the RON gene promotes invasive growth but not transformation.
Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 39 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 88 citations in OpenAlex.
- Review
- RON in hepatobiliary and pancreatic cancers: Pathogenesis and potential therapeutic targets.World journal of gastroenterology · 2021Review
- Macrophage-Stimulating Protein Enhances Osteoblastic Differentiation via the Recepteur d'Origine Nantais Receptor and Extracellular Signal-Regulated Kinase Signaling Pathway.Journal of bone metabolism · 2020Article
- Role of Recepteur D'origine Nantais on Gastric Cancer Development and Progression.Chonnam medical journal · 2017Review
- Article
- Characterization of RON protein isoforms in pancreatic cancer: implications for biology and therapeutics.Oncotarget · 2016Article
- Roles of c-Met and RON kinases in tumor progression and their potential as therapeutic targets.Oncotarget · 2015Review
- Autoinhibition of the Ron receptor tyrosine kinase by the juxtamembrane domain.Cell communication and signaling : CCS · 2014Article
- The RON receptor tyrosine kinase promotes metastasis by triggering MBD4-dependent DNA methylation reprogramming.Cell reports · 2014Article
- Pathogenesis of RON receptor tyrosine kinase in cancer cells: activation mechanism, functional crosstalk, and signaling addiction.Journal of biomedical research · 2013Review
- MSP-RON signalling in cancer: pathogenesis and therapeutic potential.Nature reviews. Cancer · 2013Review
- Met interacts with EGFR and Ron in canine osteosarcoma.Veterinary and comparative oncology · 2013Article
- Macrophage-stimulating protein and calcium homeostasis in zebrafish.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- The growth factor SVH-1 regulates axon regeneration in C. elegans via the JNK MAPK cascade.Nature neuroscience · 2012Article
- Deletion or insertion in the first immunoglobulin-plexin-transcription (IPT) domain differentially regulates expression and tumorigenic activities of RON receptor Tyrosine Kinase.Molecular cancer · 2010Article
- Met-related receptor tyrosine kinase Ron in tumor growth and metastasis.Advances in cancer research · 2008Review
- Human RON receptor tyrosine kinase induces complete epithelial-to-mesenchymal transition but causes cellular senescence.Biochemical and biophysical research communications · 2007Article
- Ron-receptor tyrosine kinase in tumorigenesis and metastasis.Future oncology (London, England) · 2007Review
- Current understanding of the molecular mechanisms of kidney cancer: a primer for urologists.Canadian Urological Association journal = Journal de l'Association des urologues du Canada · 2007Article
- Review
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MET, RON, and SEA are members of a gene family encoding tyrosine kinase receptors with distinctive properties. Besides mediating growth, they control cell dissociation, motility ("scattering"), and formation of branching tubules. While there are transforming counterparts of MET and SEA, no oncogenic forms of RON have yet been identified. A chimeric Tpr-Ron, mimicking the oncogenic form of Met (Tpr-Met) was generated to investigate its transforming potential. For comparison, a chimeric Tpr-Sea was also constructed. Fusion with Tpr induced constitutive activation of the Ron and Sea kinases. While Tpr-Sea was more efficient than Tpr-Met in transformation, Tpr-Ron did not transform NIH 3T3 cells. The differences in the transforming abilities of Tpr-Met and Tpr-Ron were linked to the functional features of the respective tyrosine kinases using the approach of swapping subdomains. Kinetic analysis showed that the catalytic efficiency of Tpr-Ron is five times lower than that of Tpr-Met. Moreover, constitutive activation of Ron resulted in activation of the MAP kinase signaling cascade approximately three times lower than that attained by Tpr-Met. However, constitutive activation of Ron did induce a mitogenic-invasive response, causing cell dissociation, motility, and invasion of extracellular matrices. Tpr-Ron also induced formation of long, unbranched tubules in tridimensional collagen gels. These data show that RON has the potential to elicit a motile-invasive rather than a transformed phenotype.
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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.