ArticleClinical and translational medicine2014
Targeting met mediated epithelial-mesenchymal transition in the treatment of breast cancer.
Article in Clinical and translational medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
16 citing papers in PubMed, 23 citations in OpenAlex.
- MEK inhibitor mirdametinib promotes fracture healing in osteofibrous dysplasia RASopathy.The Journal of clinical investigation · 2026Article
- MET fusions and splicing variants in glioma: a landscape integrating clinical, pathological, and survival features.The journal of pathology. Clinical research · 2026Article
- Advancements in cancer biomarker discovery over fifteen years: diagnostics and prognostic approach in somatic cancer.Oncology reviews · 2026Review
- Synthesis, Anticancer Activity, and Docking Studies of Novel Hydroquinone-Chalcone-Pyrazoline Hybrid Derivatives.International journal of molecular sciences · 2024Article
- Deubiquitinase BRCC3 promotes the migration, invasion and EMT progression of colon adenocarcinoma by stabilizing MET expression.Genes & genomics · 2024Article
- 2-Acetyl-5,8-dihydro-6-(4-methyl-3-pentenyl)-1,4-naphthohydroquinone-Derived Chalcones as Potential Anticancer Agents.Molecules (Basel, Switzerland) · 2023Article
- IFITM3 promotes malignant progression, cancer stemness and chemoresistance of gastric cancer by targeting MET/AKT/FOXO3/c-MYC axis.Cell & bioscience · 2022Article
- Regulatory roles of osteopontin in human lung cancer cell epithelial-to-mesenchymal transitions and responses.Clinical and translational medicine · 2021Article
- Beta-Tocotrienol Exhibits More Cytotoxic Effects than Gamma-Tocotrienol on Breast Cancer Cells by Promoting Apoptosis via a P53-Independent PI3-Kinase Dependent Pathway.Biomolecules · 2020Article
- TBL1XR1 is involved in c-Met-mediated tumorigenesis of human nonsmall cell lung cancer.Cancer gene therapy · 2020Observational
- Review
- MicroRNA‑200a suppresses migration and invasion and enhances the radiosensitivity of NSCLC cells by inhibiting the HGF/c‑Met signaling pathway.Oncology reports · 2019Article
- New insights into the mechanisms of epithelial-mesenchymal transition and implications for cancer.Nature reviews. Molecular cell biology · 2019Review
- A Model-System to Address the Impact of Phenotypic Heterogeneity and Plasticity on the Development of Cancer Therapies.Frontiers in oncology · 2019Article
- Molecular mechanism of anti-cancer activity of phycocyanin in triple-negative breast cancer cells.BMC cancer · 2015Article
- Therapeutic Implications of Cellular Heterogeneity and Plasticity in Breast Cancer.Cell stem cell · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mesenchymal epithelial transition factor receptor (Met) is a receptor tyrosine kinase that plays a critical role in promoting cancer cell malignant progression. Met is activated by its ligand hepatocyte growth factor (HGF). HGF-dependent Met activation plays an important role in stimulating epithelial-mesenchymal transition (EMT) in tumor cells, resulting in increased tumor cell proliferation, survival, motility, angiogenesis, invasion, and metastasis. The HGF/Met axis has thus attracted great interest as a potential target in the development of novel cancer therapies. In an effort to suppress tumor cell malignant progression, efforts have been made to develop agents capable of inhibiting inhibit Met-induced EMT, including specific Met tyrosine kinase inhibitors, HGF antagonists that interfere with HGF binding to Met, and antibodies that prevent Met activation and/or dimerization. Tocotrienols, a subgroup within the vitamin E family of compounds, display potent anticancer activity that results, at least in part, from inhibition of HGF-dependent Met activation and signaling. The present review will provide a brief summary of the increasing importance of the HGF/Met axis as an attractive target for cancer chemotherapy and the role of tocotrienols in suppressing Met activation, signaling and HGF-induced EMT in breast cancer cells. Evidence provided suggests that γ-tocotrienol therapy may afford significant benefit in the treatment of breast cancers characterized by Met dysregulation.
Indexed as
Identifiers
What OpenQuestion holds
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.