ArticleCells2025
Metformin Inhibits Cell Motility and Proliferation of Triple-Negative Breast Cancer Cells by Blocking HMGB1/RAGE Signaling.
Article in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Deciphering the Anti-Tumor Mechanisms of Metformin Through Reprogramming of the Tumor Microenvironment.Cells · 2026Review
- Spatiotemporal heterogeneity of neutrophil extracellular traps in hepatocellular carcinoma microenvironment and targeted therapy progress.Journal of translational medicine · 2026Review
- The Role of the HMGB1 C-Terminal Domain in Epithelial-Mesenchymal Transition and Invasion in 2D and 3D MDA-MB-231 Breast Cancer Models.International journal of molecular sciences · 2026Article
- Celastrol increases anoikis sensitivity to suppress triple-negative breast cancer via EGFR pathway and p-EMT state regulation.Frontiers in pharmacology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
High-mobility group box 1 (HMGB1) is a nuclear chromatin protein overexpressed in various cancers and linked to tumor progression. Outside the cell, HMGB1 binds to receptors such as the receptor for advanced glycation end products (RAGE), promoting metastasis. Targeting this signaling pathway may provide a new therapeutic strategy for aggressive cancers. Metformin, a well-established antidiabetic drug, directly interacts with HMGB1, inhibiting its pro-inflammatory functions. This study investigates metformin's effects on the HMGB1/RAGE signaling pathway in triple-negative breast cancer (TNBC) cells. Using wound-healing and colony formation assays, we demonstrate that metformin reduces HMGB1-induced cell migration and proliferation. Immunoblotting and immunofluorescence analyses reveal that metformin decreases RAGE stabilization on the cell membrane, disrupts NF-κB signaling, and reverses the epithelial-to-mesenchymal transition (EMT) by increasing E-cadherin, reducing vimentin, and stabilizing β-catenin at the cell membrane. Furthermore, metformin lowers HMGB1 and RAGE protein levels, disrupting the positive feedback loop that promotes cancer aggressiveness. These findings highlight metformin's potential as a therapeutic agent in TNBC by inhibiting HMGB1/RAGE-driven metastasis.
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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.