ArticleOncology letters2016
Curcumin mediates reversion of HGF-induced epithelial-mesenchymal transition via inhibition of c-Met expression in DU145 cells.
Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses 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.
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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
25 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Pooled it
- Systematic review of the old and new concepts in the epithelial-mesenchymal transition of colorectal cancer.World journal of gastroenterology · 2016Pooled it
- Medicinal Chemistry of Small-Molecule c-Met Inhibitors: From Approved Therapies to Emerging Multitarget Anticancer Agents.International journal of molecular sciences · 2026Review
- Green-SynthesizedJournal of functional biomaterials · 2026Article
- Anti-Leukemic Properties of Curcumin on Acute Lymphoblastic Leukemia: A Systematic Review.Biology · 2026Review
- Bioactive Products Targeting C-Met As Potential Antitumour Drugs.Anti-cancer agents in medicinal chemistry · 2025Review
- A map of signaling responses in the human airway epithelium.Cell systems · 2024Article
- Targeting c-Met in the treatment of urologic neoplasms: Current status and challenges.Frontiers in oncology · 2023Review
- Monocarbonyl Curcumin Analogues as Potent Inhibitors against Human Glutathione Transferase P1-1.Antioxidants (Basel, Switzerland) · 2022Article
- Cetuximab resistance induced by hepatocyte growth factor is overcome by MET inhibition in KRAS, NRAS, and BRAF wild-type colorectal cancers.Journal of cancer research and clinical oncology · 2022Article
- Article
- Mechanistic Pathogenesis of Endothelial Dysfunction in Diabetic Nephropathy and Retinopathy.Frontiers in endocrinology · 2022Review
- Receptor Tyrosine Kinases and Their Signaling Pathways as Therapeutic Targets of Curcumin in Cancer.Frontiers in pharmacology · 2021Review
- Curcumin against Prostate Cancer: Current Evidence.Biomolecules · 2020Review
- Identification of HGF as a novel target of miR-15a/16/195 in gastric cancer.Investigational new drugs · 2020Article
- Resveratrol Suppresses Prostate Cancer Epithelial Cell Scatter/Invasion by Targeting Inhibition of Hepatocyte Growth Factor (HGF) Secretion by Prostate Stromal Cells and Upregulation of E-cadherin by Prostate Cancer Epithelial Cells.International journal of molecular sciences · 2020Article
- Crosstalk between tubular epithelial cells and glomerular endothelial cells in diabetic kidney disease.Cell proliferation · 2020Review
- Natural Compounds in Prostate Cancer Prevention and Treatment: Mechanisms of Action and Molecular Targets.Cells · 2020Review
- Integrative Informatics Analysis of Transcriptome and Identification of Interacted Genes in the Glomeruli and Tubules in CKD.Frontiers in medicine · 2020Article
- Curcumin: a potent agent to reverse epithelial-to-mesenchymal transition.Cellular oncology (Dordrecht, Netherlands) · 2019Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hepatocyte growth factor (HGF)/c-Met signaling pathway results in cancer cell scattering and invasion, and has been reported to participate in several types of cancer, including prostate and colorectal cancer. The downstream phosphorylation cascade of HGF, particularly the mitogen-activated protein kinase and phosphoinositide 3-kinase/AKT signaling pathway, regulates epithelial-mesenchymal transition (EMT). However, the mechanism by which these signaling pathways govern EMT, and whether certain kinases are able to respond to specific EMT effectors, remains to be elucidated. In the present study, an increase in the levels of vimentin, rather than co-regulation of certain EMT marker proteins, was observed in response to HGF-induced EMT in DU145 prostate cancer cells. In addition, it was observed that curcumin abrogated HGF-induced DU145 cell scattering and invasion. Furthermore, curcumin was able to effectively inhibit the HGF-induced increase in the levels of vimentin by downregulating the expression of phosphorylated c-Met, extracellular signal-regulated kinase and Snail. In conclusion, the results of the present study demonstrated that curcumin was able to reverse HGF-induced EMT, possibly by inhibiting c-Met expression in DU145 prostate cancer cells.
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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.