ReviewCell communication and signaling : CCS2017
c-Met expression and activity in urogenital cancers - novel aspects of signal transduction and medical implications.
Review in Cell communication and signaling : CCS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07549061 (A Phase II Study of Vebreltinib Combined With Platinum-Doublet Chemotherapy as First-Line Treatment for Locally Advanced or Metastatic Non-Small Cell Lung Cancer), which is not on this 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.
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.
A Phase II Study of Vebreltinib Combined With Platinum-Doublet Chemotherapy as First-Line Treatment for Locally Advanced or Metastatic Non-Small Cell Lung Cancer (NSCLC) With Negative Driver Genes and MET Overexpression
Who cites it
19 citing papers in PubMed.
- Article
- The role and research progress of the MET signalling pathway in targeted therapy for osteosarcoma.Oncology reviews · 2025Review
- Expressions and Clinical Significance of Met and YAP in Gastric Cancer Tissue Microarray.Gastroenterology research and practice · 2024Article
- Liposomal Nanoformulation as a Carrier for Curcumin and pEGCG-Study on Stability and Anticancer Potential.Nanomaterials (Basel, Switzerland) · 2022Article
- Opportunities and challenges of targeting c-Met in the treatment of digestive tumors.Frontiers in oncology · 2022Review
- c-Met: A Promising Therapeutic Target in Bladder Cancer.Cancer management and research · 2022Review
- Hepatocyte growth factor and soluble cMet levels in plasma are prognostic biomarkers of mortality in patients with severe acute kidney injury.Kidney research and clinical practice · 2021Article
- Dynamin 3 Inhibits the Proliferation of Non-small-Cell Lung Cancer Cells by Suppressing c-MET-GBR2-STAT3 Complex Formation.Frontiers in cell and developmental biology · 2021Article
- Ovarian Cancer: Therapeutic Strategies to Overcome Immune Suppression.Advances in experimental medicine and biology · 2021Article
- A c-Met Inhibitor Suppresses Osteosarcoma Progression via the ERK1/2 Pathway in Human Osteosarcoma Cells.OncoTargets and therapy · 2021Article
- Article
- c-Met expression in renal cell carcinoma with bone metastases.Journal of bone oncology · 2020Review
- Pathological roles of c-Met in bladder cancer: Association with cyclooxygenase-2, heme oxygenase-1, vascular endothelial growth factor-A and programmed death ligand 1.Oncology letters · 2020Article
- Communication Of Cancer Cells And Lymphatic Vessels In Cancer: Focus On Bladder Cancer.OncoTargets and therapy · 2019Article
- Solution structure of SHIP2 SH2 domain and its interaction with a phosphotyrosine peptide from c-MET.Archives of biochemistry and biophysics · 2018Article
- Soluble cMet levels in urine are a significant prognostic biomarker for diabetic nephropathy.Scientific reports · 2018Article
- microRNA-1246 Is an Exosomal Biomarker for Aggressive Prostate Cancer.Cancer research · 2018Article
- Function of the c-Met receptor tyrosine kinase in carcinogenesis and associated therapeutic opportunities.Molecular cancer · 2018Review
- MET/SMAD3/SNAIL circuit mediated by miR-323a-3p is involved in regulating epithelial-mesenchymal transition progression in bladder cancer.Cell death & disease · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C-Met is a receptor tyrosine kinase with multiple functions throughout embryonic development, organogenesis and wound healing and is expressed in various epithelia. The ligand of c-Met is Hepatocyte Growth Factor (HGF) which is secreted among others by mesenchymal stroma/stem (MSC) cells.Physiological c-Met functions are centred around processes that underly cellular motility and invasive growth. Aberrant c-Met expression and activity is observed in numerous cancers and makes major contributions to cell malignancy. Importantly, HGF/c-Met signaling is crucial in the context of communication between cancer cells and the the tumor stroma.Here, we review recent findings on roles of dysregulated c-Met in urogenital tumors such as cancers of the urinary bladder, prostate, and ovary. We put emphasis on novel aspects of cancer-associated c-Met expression regulation on both, HGF-dependent and HGF-independent non-canonical mechanisms. Moreover, this review focusses on c-Met-triggered signalling with potential relevance for urogenital oncogenesis, and on strategies to specifically inhibit c-Met activity.
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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.