ArticleProceedings of the National Academy of Sciences of the United States of America2001
Suppression of Ras-mediated tumorigenicity and metastasis through inhibition of the Met receptor tyrosine kinase.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
- Guidelines for biomarker testing in metastatic melanoma: a National Consensus of the Spanish Society of Pathology and the Spanish Society of Medical Oncology.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2014Guideline
- The immunotherapy era in ovarian clear cell carcinoma: current evidence and future perspective.Frontiers in immunology · 2025Review
- Review the progression of ovarian clear cell carcinoma from the perspective of genomics and epigenomics.Frontiers in genetics · 2023Review
- Review
- c-Met expression in renal cell carcinoma with bone metastases.Journal of bone oncology · 2020Review
- Isoform-specific Ras signaling is growth factor dependent.Molecular biology of the cell · 2019Article
- Review
- Article
- Activation of KRAS Mediates Resistance to Targeted Therapy in MET Exon 14-mutant Non-small Cell Lung Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- Analysis of progress and challenges for various patterns of c-MET-targeted molecular imaging: a systematic review.EJNMMI research · 2017Review
- A phase 1 study of the c-Met inhibitor, tivantinib (ARQ197) in children with relapsed or refractory solid tumors: A Children's Oncology Group study phase 1 and pilot consortium trial (ADVL1111).Pediatric blood & cancer · 2017Article
- Receptor tyrosine kinase Met promotes cell survival via kinase-independent maintenance of integrin α3β1.Molecular biology of the cell · 2016Article
- Monocarboxylate transporter 1 contributes to growth factor-induced tumor cell migration independent of transporter activity.Oncotarget · 2016Article
- Isothiocyanatostilbenes as novel c-Met inhibitors.Oncotarget · 2015Article
- Differential reprogramming of isogenic colorectal cancer cells by distinct activating KRAS mutations.Journal of proteome research · 2015Article
- The melanoma revolution: from UV carcinogenesis to a new era in therapeutics.Science (New York, N.Y.) · 2014Review
- Anti-tumor activity of oridonin on SNU-5 subcutaneous xenograft model via regulation of c-Met pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Four individually druggable MET hotspots mediate HGF-driven tumor progression.The Journal of clinical investigation · 2014Article
- Met degradation by SAIT301, a Met monoclonal antibody, reduces the invasion and migration of nasopharyngeal cancer cells via inhibition of EGR-1 expression.Cell death & disease · 2014Article
- MEK targeting in N-RAS mutated metastatic melanoma.Molecular cancer · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the Ras family of GTP binding proteins represent one of the most frequently observed genetic alterations in human cancers. We and others have recently demonstrated that expression of Met, the tyrosine kinase receptor for hepatocyte growth factor/scatter factor (HGF/SF), is significantly up-regulated in Ras-transformed cells. Because HGF/SF-Met signaling is proposed to play a prominent role in tumor development and progression, we assessed the possible requirement for Met during Ras-mediated tumor growth and metastasis. To disrupt endogenous Met signaling, we constructed dominant-negative mutants of both human and murine Met and showed that these can inhibit HGF/SF-mediated Met signaling and cell invasion of ras-transformed cells in vitro. Moreover, ectopic expression of dominant-negative Met mutants reduced the s.c. tumor growth of ras-transformed cells and dramatically suppressed their ability to form lung metastases in vivo. Our data demonstrate that Met plays a prominent role during Ras-mediated tumor growth and metastasis, and further suggest that agents that inhibit HGF/SF-Met signaling may represent an important therapeutic avenue for the treatment of a variety of malignant tumors.
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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.