ReviewBiomedicines2015
HGF/c-MET Axis in Tumor Microenvironment and Metastasis Formation.
Review in Biomedicines, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed.
- Targeting the NF-κB pathway represents a potential strategy to attenuate HGF-induced resistance to KRAS G12C inhibitors in lung adenocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- CAR-T cell therapy for pediatric solid tumors: armored CAR-T cells and beyond.Cancer metastasis reviews · 2026Review
- Macrophages in Colorectal Cancer: from Normal Mucosa to Distant Metastasis: Beyond the M1/M2 Paradigm.Journal of Cancer · 2026Review
- Emerging Nanoplatforms are Effective Against Tumor Hypoxia.International journal of nanomedicine · 2026Review
- Immunophenotypic changes in the tumor and tumor microenvironment during progression to multiple myeloma.PLoS genetics · 2025Article
- Development of a cyst-targeted therapy for polycystic kidney disease using an antagonistic dimeric IgA monoclonal antibody against cMET.Cell reports. Medicine · 2025Article
- Dual blockage of P-cadherin and c-Met synergistically inhibits the growth of head and neck cancer.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- HGF/c-Met Axis-Targeted Nanotherapy via GSH-Responsive Polymer Platforms Suppresses Uveal Melanoma Metastasis.Advanced healthcare materials · 2025Article
- Role of mitogens in normal and pathological liver regeneration.Hepatology communications · 2025Review
- MicroRNA-142-3p Overcomes Drug Resistance in Hepatocellular Carcinoma by Targeting YES1 and TWF1.International journal of molecular sciences · 2025Article
- Review
- Pre-metastatic niche: formation, characteristics and therapeutic implication.Signal transduction and targeted therapy · 2024Review
- The influence of xeno-free culture conditions on the angiogenic and adipogenic differentiation properties of adipose tissue-derived stem cells.Regenerative therapy · 2024Article
- Mesenchymal-epithelial transition factor amplification correlates with adverse pathological features and poor clinical outcome in colorectal cancer.World journal of gastrointestinal surgery · 2024Article
- Two Enhances the Cisplatin Sensitivity of Cervical Cancer Cells via Suppression of c-MET Expression.Iranian journal of public health · 2023Article
- Article
- MACC1-induced migration in tumors: Current state and perspective.Frontiers in oncology · 2023Review
- Prognostic value of hepatocyte growth factor for muscle-invasive bladder cancer.Journal of cancer research and clinical oncology · 2022Article
- The Antioxidant and Antitumor Efficiency ofLife (Basel, Switzerland) · 2022Article
- Anti-cancer therapeutic strategies based on HGF/MET, EpCAM, and tumor-stromal cross talk.Cancer cell international · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor metastases are responsible for approximately 90% of all cancer-related deaths. Metastasis formation is a multistep process that requires acquisition by tumor cells of a malignant phenotype that allows them to escape from the primary tumor site and invade other organs. Each step of this mechanism involves a deep crosstalk between tumor cells and their microenvironment where the host cells play a key role in influencing metastatic behavior through the release of many secreted factors. Among these signaling molecules, Hepatocyte Growth Factor (HGF) is released by many cell types of the tumor microenvironment to target its receptor c-MET within the cells of the primary tumor. Many studies reveal that HGF/c-MET axis is implicated in various human cancers, and genetic and epigenetic gain of functions of this signaling contributes to cancer development through a variety of mechanisms. In this review, we describe the specific types of cells in the tumor microenvironment that release HGF in order to promote the metastatic outgrowth through the activation of extracellular matrix remodeling, inflammation, migration, angiogenesis, and invasion. We dissect the potential use of new molecules that interfere with the HGF/c-MET axis as therapeutic targets for future clinical trials in cancer disease.
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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.