ArticleOncology letters2018
Metformin inhibits the proliferation and metastasis of osteosarcoma cells by suppressing the phosphorylation of Akt.
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 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Comparison of Metformin Combinations with Other Repurposed Drugs in the Treatment of Hamster Fibrosarcoma: A Review.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Targeting metastasis in paediatric bone sarcomas.Molecular cancer · 2025Review
- Metformin and the PI3K/AKT signaling pathway: implications for cancer, cardiovascular, and central nervous system diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Metformin alleviates adriamycin resistance of osteosarcoma by declining YY1 to inhibit MDR1 transcriptional activity.BMC pharmacology & toxicology · 2023Article
- Metformin sensitises osteosarcoma to chemotherapy <em>via</em> the IGF-1R/miR-610/FEN1 pathway.European journal of histochemistry : EJH · 2023Article
- Metformin in aging and aging-related diseases: clinical applications and relevant mechanisms.Theranostics · 2022Review
- Insight into the interplay between mitochondria-regulated cell death and energetic metabolism in osteosarcoma.Frontiers in cell and developmental biology · 2022Review
- The Effect of Metformin on the Clinicopathological Features of Breast Cancer With Type 2 Diabetes.World journal of oncology · 2020Article
- Metformin Inhibited Proliferation and Metastasis of Colorectal Cancer and presented a Synergistic Effect on 5-FU.BioMed research international · 2020Article
- Anticancer activity of metformin: a systematic review of the literature.Future science OA · 2019Review
- 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
- Metformin Suppresses Self-Renewal Ability and Tumorigenicity of Osteosarcoma Stem Cells via Reactive Oxygen Species-Mediated Apoptosis and Autophagy.Oxidative medicine and cellular longevity · 2019Article
- Pleiotropic Effects of Metformin on Cancer.International journal of molecular sciences · 2018Review
- Molecular Mechanisms of Metformin for Diabetes and Cancer Treatment.Frontiers in physiology · 2018Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metformin (Met) is a therapeutic agent for the treatment of type 2 diabetes mellitus. There is evidence that Met may reduce the risk of cancer in patients with type 2 diabetes mellitus by inhibiting tumor cell growth, prolonging the overall survival time in patients with various types of malignancy. However, the function and mechanism of Met have not been fully elucidated in osteosarcoma (OS). The present study evaluated the anti-proliferative effect of Met on MG63 and U2OS OS cells, identifying that it acted in a dose- and time-dependent manner. Met also inhibited OS cell migration and invasion, potentially by regulating the epithelial-mesenchymal transition in OS cells. Mechanistically, Met was demonstrated to partly exert these functions through the suppression of Akt phosphorylation, which was associated with increased phosphatase and tensin (PTEN) expression. Silencing PTEN prevented the Met-induced inhibition of the growth and metastasis of OS cells. As Met has anti-proliferative and anti-metastatic effects on OS cells it is a potential candidate, in combination with other chemotherapeutic agents, for use in the treatment of OS.
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Registered trials
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