ArticleScientific reports2019
Metformin prevention of doxorubicin resistance in MCF-7 and MDA-MB-231 involves oxidative stress generation and modulation of cell adaptation genes.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
42 citing papers in PubMed, 96 citations in OpenAlex.
- Comparative Effects of Metformin, Boric Acid, and Lithium Chloride on Oxidative Stress-Mediated Cytotoxicity in HepG2 Hepatocarcinoma Cells.Biological trace element research · 2026Article
- Antineoplastic effect of piperine compared with doxorubicin via suppressing γ-secretase/notch pathway in breast cancer cells.Discover oncology · 2026Article
- Radionuclide-stimulated dynamic therapy induces complementary immunogenic necroptosis and apoptosis cancer cell death pathways.Communications biology · 2026Article
- HERPUD1 mediates palmitic acid-induced UPR sustaining TNBC aggressiveness and is destabilized by CK2 pharmacological inhibition.Cell death & disease · 2025Article
- Redox Balance in Cancer in the Context of Tumor Prevention and Treatment.Biomedicines · 2025Review
- PRR13 expression as a prognostic biomarker in breast cancer: correlations with immune infiltration and clinical outcomes.Frontiers in molecular biosciences · 2025Article
- cRGD-Peptide Modified Covalent Organic Frameworks for Precision Chemotherapy in Triple-Negative Breast Cancer.ACS applied materials & interfaces · 2024Article
- Changes in the Sensitivity of MCF-7 and MCF-7/DX Breast Cancer Cells to Cytostatic in the Presence of Metformin.Molecules (Basel, Switzerland) · 2024Article
- Acetylcytidine modification of DDX41 and ZNF746 byFrontiers in oncology · 2024Article
- Carborane-Based ABCG2-Inhibitors Sensitize ABC-(Over)Expressing Cancer Cell Lines for Doxorubicin and Cisplatin.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Metformin and Aspirin: Anticancer effects on A549 and PC3 cancer cells and the mechanisms of action.Toxicology research · 2023Article
- The Effects of a Curcumin Derivative and Osimertinib on Fatty Acyl Metabolism and Mitochondrial Functions in HCC827 Cells and Tumors.International journal of molecular sciences · 2023Article
- HERPUD1, a Member of the Endoplasmic Reticulum Protein Quality Control Mechanism, may be a Good Target for Suppressing Tumorigenesis in Breast Cancer Cells.Turkish journal of pharmaceutical sciences · 2023Article
- Upregulation of NUAK2: A novel prognostic marker in breast cancer.Histology and histopathology · 2023Article
- Article
- Article
- Interpretable Machine Learning Models to Predict the Resistance of Breast Cancer Patients to Doxorubicin from Their microRNA Profiles.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Mitochondrial adaptation in cancer drug resistance: prevalence, mechanisms, and management.Journal of hematology & oncology · 2022Review
- Metformin counteracts stimulatory effects induced by insulin in primary breast cancer cells.Journal of translational medicine · 2022Article
- Synergy between sublethal doses of shikonin and metformin fully inhibits breast cancer cell migration and reverses epithelial-mesenchymal transition.Molecular biology reports · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metformin was shown to sensitize multidrug resistant breast cancer cells; however, the mechanisms involved in this capacity need to be clarified. We investigated oxidative stress and inflammatory-related pathways during the induction of doxorubicin resistance in MCF-7 and MDA-MB-231 human breast cancer cells (DOX-res group), and evaluated metformin-induced cellular responses that resulted in the prevention of doxorubicin resistance (Met-DOX group). Microarray analysis demonstrated that DOX-res changed the expression of genes involved in oxidative stress (OS) and the TGF- β1 pathway. The DOX-res group presented increased thiols and reduced lipoperoxidation, increased levels of nitric oxide, nuclear NF-kB and Nrf2, and reduced nuclear p53 labelling. Analysis of the TGF-β1 signaling pathway by RT-PCR array showed that DOX-res developed adaptive responses, such as resistance against apoptosis and OS. Metformin treatment modified gene expression related to OS and the IFN-α signaling pathway. The Met-DOX group was more sensitive to DOX-induced OS, presented lower levels of nitric oxide, nuclear NF-kB and Nrf2, and increased nuclear p53. Analysis of the IFN-α signaling pathway showed that Met-DOX presented more sensitivity to apoptosis and OS. Our findings indicate that metformin is a promising tool in the prevention of chemoresistance in patients with breast cancer submitted to doxorubicin-based treatments.
Indexed as
Identifiers
What OpenQuestion holds
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.