ArticleOncogene2006
Pro-metastatic signaling by c-Met through RAC-1 and reactive oxygen species (ROS).
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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.
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Who cites it
46 citing papers in PubMed, 131 citations in OpenAlex.
- Mitophagy's impacts on cancer and neurodegenerative diseases: implications for future therapies.Journal of hematology & oncology · 2025Review
- AIMP1: multifunctional regulator in physiology and pathology with therapeutic implications.PeerJ · 2025Review
- Hyaluronan and Reactive Oxygen Species Signaling-Novel Cues from the Matrix?Antioxidants (Basel, Switzerland) · 2023Review
- Involvement of redox signalling in tumour cell dormancy and metastasis.Cancer metastasis reviews · 2023Review
- The gate to metastasis: key players in cancer cell intravasation.The FEBS journal · 2022Review
- The Dark Side of Melanin Secretion in Cutaneous Melanoma Aggressiveness.Frontiers in oncology · 2022Review
- Lipid Metabolism Regulates Oxidative Stress and Ferroptosis in RAS-Driven Cancers: A Perspective on Cancer Progression and Therapy.Frontiers in molecular biosciences · 2021Review
- A Perspective on Therapeutic Pan-Resistance in Metastatic Cancer.International journal of molecular sciences · 2020Review
- Plasma Treatment Limits Human Melanoma Spheroid Growth and Metastasis Independent of the Ambient Gas Composition.Cancers · 2020Article
- Peroxynitrite promotes serine-62 phosphorylation-dependent stabilization of the oncoprotein c-Myc.Redox biology · 2020Article
- Metabolic reprogramming and cancer progression.Science (New York, N.Y.) · 2020Review
- Mitochondrial Haplotype of the Host Stromal Microenvironment Alters Metastasis in a Non-cell Autonomous Manner.Cancer research · 2020Article
- Understanding and Modeling Metastasis Biology to Improve Therapeutic Strategies for Combating Osteosarcoma Progression.Frontiers in oncology · 2020Review
- Flura-seq identifies organ-specific metabolic adaptations during early metastatic colonization.eLife · 2019Article
- HGF/c-MET Signaling in Melanocytes and Melanoma.International journal of molecular sciences · 2018Review
- ROS-modulated therapeutic approaches in cancer treatment.Journal of cancer research and clinical oncology · 2017Review
- Article
- Potential Antitumor Activity of SIM-89 in Non-Small Cell Lung Cancer Cells.Yonsei medical journal · 2017Article
- Genetic Nrf2 Overactivation Inhibits the Deleterious Effects Induced by Hepatocyte-Specific c-met Deletion during the Progression of NASH.Oxidative medicine and cellular longevity · 2017Article
- Different growth and metastatic phenotypes associated with a cell-intrinsic change of Met in metastatic melanoma.Oncotarget · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression of the c-Met/hepatocyte growth factor receptor(HGF-R) proto-oncogene and abnormal generation of intracellular oxygen species (reactive oxygen species (ROS)) have been linked, by independent lines of evidence, to cell transformation and to malignant growth. By comparing two subpopulations of the B16 mouse melanoma (B16-F0 and B16-F10) endowed with different lung metastasis capacities (low and high, respectively) we found that both the expression/phosphorylation of c-Met and the steady-state levels of ROS positively correlated with metastatic growth. shRNA-mediated downregulation of c-Met in F10 cells led to a parallel decrease in the generation of oxygen species and in metastatic capacity, suggesting that oxidants may mediate the pro-metastatic activity of the HGF receptor. c-Met activation by a ligand elicits the formation of oxidant species through the oxidase-coupled small GTPase Rac-1, a relevant downstream target of the HGF-R. Moreover, cell treatment with the catalytic ROS scavengers EUK-134 and EUK-189 attenuates Met signaling to ERKs and inhibits the anchorage-independent growth of F10 cells, consistent with a critical role for oxygen species in HGF signaling and in aggressive cell behavior. Finally, genetic manipulation of the Rac-ROS cascade at different levels demonstrated its crucial role in the pro-metastatic activity of c-Met in vivo. Thus, we have outlined a novel cascade triggered by c-Met and mediated by ROS, linked to metastasis and potentially targetable by new antimetastatic, redox-based therapies.
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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.