ArticleOncotarget2017
Metformin reverses bFGF-induced epithelial-mesenchymal transition in HCC cells.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Unveiling the impacts of metformin on hepatocellular carcinoma: A bioinformatic exploration in cell lines.Narra J · 2024Article
- Review
- Review
- High-level transient production of a protease-resistant mutant form of human basic fibroblast growth factor inPlant biotechnology (Tokyo, Japan) · 2022Article
- Astaxanthin Prevents Diet-Induced NASH Progression by Shaping Intrahepatic Immunity.International journal of molecular sciences · 2021Article
- Bleomycin induces epithelial-to-mesenchymal transition via bFGF/PI3K/ESRP1 signaling in pulmonary fibrosis.Bioscience reports · 2020Article
- Honokiol inhibits breast cancer cell metastasis by blocking EMT through modulation of Snail/Slug protein translation.Acta pharmacologica Sinica · 2019Article
- Metformin reverses mesenchymal phenotype of primary breast cancer cells through STAT3/NF-κB pathways.BMC cancer · 2019Article
- The Role of AMP-Activated Protein Kinase as a Potential Target of Treatment of Hepatocellular Carcinoma.Cancers · 2019Review
- Epithelial Mesenchymal and Endothelial Mesenchymal Transitions in Hepatocellular Carcinoma: A Review.BioMed research international · 2019Review
- Proteomic Technology "Lens" for Epithelial-Mesenchymal Transition Process Identification in Oncology.Analytical cellular pathology (Amsterdam) · 2019Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metformin had exerted important inhibitory effects in multiple cancers. However, the correlation between metformin and hepatocellular carcinoma (HCC) metastasis, and the relevant mechanisms are still unclear. By quantitative proteomics analysis technique, we found metformin could suppress FGF signalling significantly. In FGF signalling basic fibroblast growth factor (bFGF) is a crucial member, it initially binds to its receptors, the complex of bFGF and receptors activate FGF signallings, and promote many cancers progressions. When treating HCC cell lines HepG2 and Huh7 with bFGF, we observed the cells exhibited epithelial mesenchymal transition (EMT) and these cells metastasis potential was enhanced dramaticlly. However, when treating with metformin and bFGF together, EMT and metastasis induced by bFGF could be inhibited in these cells. Furthermore, bFGF could activate AKT/GSK-3β signalling, sequentially decrease the interaction between GSK-3β and Twist1 and decrease ubiquitination of Twist1 leading to Twist1 degradation reducing. While metformin could repress the bFGF-mediated activation in AKT/GSK-3β signalling, inhibition on interaction between GSK-3β and Twist1, enhancement of Twist1 stability. Taken together, our findings suggested that metformin had prominent negative effects on bFGF-induced EMT and metastasis in HCC cells.
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Registered trials
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