ArticleGene therapy2004
Inhibition of human non-small cell lung tumors by a c-Met antisense/U6 expression plasmid strategy.
Article in Gene therapy, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 46 citations in OpenAlex.
- Hepatocyte growth factor/c-Met signaling axis in human diseases: Mechanistic insights and therapeutic potential.Journal of cell communication and signaling · 2026Review
- Systematic review of c-met as a prognostic indicator in esophageal cancer patients: a meta-analysis study.Discover oncology · 2025Article
- c-Met as a Target for Personalized Therapy.Translational oncogenomics · 2015Review
- Phosphotyrosine profiling of NSCLC cells in response to EGF and HGF reveals network specific mediators of invasion.Journal of proteome research · 2013Article
- HGF-independent potentiation of EGFR action by c-Met.Oncogene · 2011Article
- DNA triplex-mediated inhibition of MET leads to cell death and tumor regression in hepatoma.Cancer gene therapy · 2011Article
- Inhibition of c-Met downregulates TIGAR expression and reduces NADPH production leading to cell death.Oncogene · 2011Article
- Article
- HGF and c-Met participate in paracrine tumorigenic pathways in head and neck squamous cell cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Article
- Role of transglutaminase 2 in liver injury via cross-linking and silencing of transcription factor Sp1.Gastroenterology · 2009Article
- MET as a target for treatment of chest tumors.Lung cancer (Amsterdam, Netherlands) · 2009Review
- Insulin-like growth factor-1 receptor-targeted therapy for non-small cell lung cancer: a mini review.American journal of translational research · 2009Article
- Therapeutic targeting of human hepatocyte growth factor with a single neutralizing monoclonal antibody reduces lung tumorigenesis.Molecular cancer therapeutics · 2008Article
- Inhibition of c-Met as a therapeutic strategy for esophageal adenocarcinoma.Neoplasia (New York, N.Y.) · 2006Article
- The future of antisense oligonucleotides in the treatment of respiratory diseases.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2006Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
c-Met is a receptor tyrosine kinase whose activation by hepatocyte growth factor (HGF) can lead to transformation and tumorigenicity in a variety of tumors. We investigated the effects of suppressing c-Met protein expression in human non-small cell lung tumors. Expression plasmids containing either sense or antisense sequences of the human c-met gene were constructed under control of the U6 snRNA promoter. A U6 control plasmid was also constructed that did not contain any c-met sequence. These constructs have been examined both in vitro and in an in vivo tumor xenograft model. The c-Met protein was downregulated by 50-60% in two lung cancer cell lines that were transiently transfected with the c-Met antisense versus U6 control. Tumor cells treated with the c-Met antisense construct also show decreased phosphorylation of c-Met and MAP kinase when exposed to exogenous HGF. Lung cancer cells were grown as xenografts in mice and treated by intratumoral liposome-mediated transfer of the c-Met sense, antisense or U6 control plasmids. The treatment of lung tumors with c-Met antisense versus U6 control plasmid resulted in the downregulation of the c-Met protein expression, a 50% decrease in tumor growth over a 5-week treatment period and an increased rate of apoptosis. These results suggest that targeting the HGF/c-Met pathway may be an effective novel strategy to treat lung cancer patients.
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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.