ArticleJournal of cellular and molecular medicine2020
Metformin suppresses proliferation and invasion of drug-resistant breast cancer cells by activation of the Hippo pathway.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Antiproliferative Mechanisms of Metformin in Breast Cancer: A Systematic Review of the Literature.International journal of molecular sciences · 2024Pooled it
- Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer.Molecular oncology · 2026Review
- WWC proteins as emerging biomarkers and therapeutic targets in cancer pathogenesis.Frontiers in cell and developmental biology · 2026Review
- Article
- Metformin-Induced Apoptosis Is Mediated Through Mitochondrial VDAC1.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Review
- Decoding gene expression profiles of Hippo signaling pathway components in breast cancer.Molecular biology reports · 2025Article
- Investigation of potential anti-metastatic effect of metformin and caffeic acid combination therapy in breast cancer cell line in in-vitro culture model.Medical oncology (Northwood, London, England) · 2025Article
- Metformin as a PotentialInternational journal of breast cancer · 2024Review
- The NDR family of kinases: essential regulators of aging.Frontiers in molecular neuroscience · 2024Review
- Low dosage combination treatment with metformin and simvastatin inhibits obesity-promoted pancreatic cancer development in male KrasG12D mice.Scientific reports · 2023Article
- AMPK-Dependent YAP Inhibition Mediates the Protective Effect of Metformin against Obesity-Associated Endothelial Dysfunction and Inflammation.Antioxidants (Basel, Switzerland) · 2023Article
- Article
- Insights on the role of anti-inflammatory and immunosuppressive agents in the amelioration of diabetes.Diabetology international · 2023Review
- Metformin and simvastatin synergistically suppress endothelin 1-induced hypoxia and angiogenesis in multiple cancer types.Cancer science · 2023Article
- Action Mechanism of Metformin and Its Application in Hematological Malignancy Treatments: A Review.Biomolecules · 2023Review
- Evaluation of Quantification and Normalization Strategies for Phosphoprotein Phosphatase Affinity Proteomics: Application to Breast Cancer Signaling.Journal of proteome research · 2023Article
- High-accuracy prediction of colorectal cancer chemotherapy efficacy using machine learning applied to gene expression data.Frontiers in physiology · 2023Article
- KLF2 is a clinical diagnostic and treatment biomarker of breast cancer.Frontiers in cell and developmental biology · 2023Article
- Genetic Alterations and Deregulation of Hippo Pathway as a Pathogenetic Mechanism in Bone and Soft Tissue Sarcoma.Cancers · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug resistance limits the clinical efficacy of breast cancer therapies, and overexpression or activation of Yes-associated protein (YAP) is common in drug-resistant cancer cells. Thus, inhibition of YAP may reduce resistance to anti-cancer drugs. Metformin (MET), a first-line diabetes medication that also has anti-tumour activities, induces AMP-activated protein kinase (AMPK), directly phosphorylates YAP and inhibits YAP transcriptional activity. In this study, we determined the effect of MET on the proliferation and invasion of drug-resistant breast cancer cells and then investigated the underlying molecular mechanism. Our in vivo and in vitro experiments indicated that MET suppressed breast cancer by an AMPK-independent pathway to decrease YAP nuclear localization. In drug-sensitive cells, MET activated the Hippo pathway by increasing KIBRA and FRMD6 expression, but this did not occur in drug-resistant cells. Scribble (SCRIB), a cell polarity protein, was notably down-regulated in tamoxifen- and paclitaxel-resistant breast cancer cells relative to sensitive cells. We also found that MET suppressed the proliferation and invasion of drug-resistant breast cancer cells by increasing the expression and cell membrane localization of SCRIB, which enhanced the interaction of SCRIB with MST1 and LATS1, and inhibited YAP nuclear localization and transcriptional activity.
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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.