ArticleOncology letters2018
Metformin inhibits the migration and invasion of esophageal squamous cell carcinoma cells by downregulating the protein kinase B signaling pathway.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Metformin in gastrointestinal cancers and inflammatory bowel disease: Unraveling its mechanisms and therapeutic applications.iScience · 2026Review
- The role of metformin in extracellular matrix-based three-dimensional cell culture Models: A mini-review on therapeutic potentials.Biochemistry and biophysics reports · 2026Review
- Current findings on the antitumor effects of metformin on esophageal squamous cell carcinoma (Review).Molecular and clinical oncology · 2024Review
- Metformin is a potential therapeutic for COVID-19/LUAD by regulating glucose metabolism.Scientific reports · 2024Article
- Metformin in Esophageal Carcinoma: Exploring Molecular Mechanisms and Therapeutic Insights.International journal of molecular sciences · 2024Review
- Editorial: New lights Through Old Windows: Metformin and Derivatives as Anti-Cancer Treatments.Frontiers in pharmacology · 2022Article
- Prognostic Significance ofDiagnostics (Basel, Switzerland) · 2021Article
- Anticancer potential of metformin: focusing on gastrointestinal cancers.Cancer chemotherapy and pharmacology · 2021Review
- Curcumol enhances the anti-tumor effects of metformin via suppressing epithelial-mesenchymal transition in triple-negative breast cancer.Annals of translational medicine · 2020Article
- The Effect of Metformin on the Clinicopathological Features of Breast Cancer With Type 2 Diabetes.World journal of oncology · 2020Article
- Anticancer activity of metformin: a systematic review of the literature.Future science OA · 2019Review
- Synergistic Enhancement of Paclitaxel-induced Inhibition of Cell Growth by Metformin in Melanoma Cells.Development & reproduction · 2019Article
- Metformin triggers the intrinsic apoptotic response in human AGS gastric adenocarcinoma cells by activating AMPK and suppressing mTOR/AKT signaling.International journal of oncology · 2019Article
- Role of p53 Family Proteins in Metformin Anti-Cancer Activities.Journal of Cancer · 2019Review
- Berberine Attenuated Proliferation, Invasion and Migration by Targeting the AMPK/HNF4α/WNT5A Pathway in Gastric Carcinoma.Frontiers in pharmacology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have suggested that metformin, a biguanide family member widely used as an oral antidiabetic drug, may inhibit proliferation and induce apoptosis in certain types of cancer cell. However, the molecular mechanisms underlying metformin-associated anticancer effects, and in particular antimetastatic effects, remain to be fully understood. The present study assessed the efficacy of metformin in inhibiting the migration and invasion of the esophageal carcinoma cell line EC109, and evaluated the effect of metformin on the protein kinase B (AKT) signaling pathway. EC109 cells were treated with 0, 5, 10 or 20 mM metformin during the logarithmic growth phase. A Transwell assay and western blot analysis revealed that metformin inhibited the migration and invasion of EC109 cells, nuclear factor-κB activation, matrix metallopeptidase 9 and N-cadherin expression in a phosphorylated-AKT dependent manner. These results suggested that metformin inhibits the migration and invasion of human esophageal carcinoma cells by suppressing AKT phosphorylation and regulating the expression of migration- and invasion-associated genes.
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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.