ArticleInternational journal of molecular and cellular medicine2021
Metformin is a Novel Suppressor for Vimentin in Human Gastric Cancer Cell Line.
Article in International journal of molecular and cellular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.
- Antiproliferative Mechanisms of Metformin in Breast Cancer: A Systematic Review of the Literature.International journal of molecular sciences · 2024Pooled it
- Metformin's multifaceted role in colorectal cancer: mechanisms of action and synergy with standard treatments.Discover oncology · 2025Review
- Polyploidy of MDA-MB-231 cells drives increased extravasation with enhanced cell-matrix adhesion.APL bioengineering · 2025Article
- Explore Key Genes and Mechanisms Involved in Colon Cancer Progression Based on Bioinformatics Analysis.Applied biochemistry and biotechnology · 2024Article
- Metformin Inhibits Zika Virus Infection in Trophoblast Cell Line.Current microbiology · 2024Article
- Intermediate Filaments in Breast Cancer Progression, and Potential Biomarker for Cancer Therapy: A Narrative Review.Breast cancer (Dove Medical Press) · 2024Review
- Effect of Metformin on the Prognosis of Gastric Cancer Patients with Type 2 Diabetes Mellitus: A Meta-Analysis Based on Retrospective Cohort Studies.International journal of endocrinology · 2023Article
- Repurposed Drugs in Gastric Cancer.Molecules (Basel, Switzerland) · 2022Review
- Mechanism Underlying Metformin Action and Its Potential to Reduce Gastric Cancer Risk.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vimentin, an intermediate filament of mesenchymal cells, is upregulated in epithelial-mesenchymal transition (EMT) and has a main role in cancer metastasis. As a new strategy to control metastatic outgrowth, EMT markers are generally inhibited using some drugs or specific siRNA. In this study, AGS gastric cancer cells were treated with metformin and vimentin-specific siRNA (vim-siRNA) for 48 h. The impact of metformin and vim-siRNA on vimentin downregulation in AGS cells were analyzed by quantitative PCR and Western blot. Following treatment with metformin and vim-siRNA, cell motility, migration and invasion abilities of AGS cells were also analyzed. The results showed that inhibition of vimentin due to metformin was comparable with the vim-siRNA. Furthermore, wound-healing and invasion assays showed a significant decrease in migration and invasion of AGS cells following metformin and vim-siRNA treatment. Our finding for the first time indicated that metformin can be an alternative to specific siRNA for inhibition of vimentin expression and migration of AGS cell line. Taken together, our data indicates that the use of metformin might have a priority to siRNA for inhibition of gastric cancer cell behaviors siRNA is more unstable and expensive than metformin, and needs special vehicles and delivery strategies for efficient transfection of cells. Further
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