ArticleOncotarget2015
Metformin represses cancer cells via alternate pathways in N-cadherin expressing vs. N-cadherin deficient cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 25 citations in OpenAlex.
- High glucose promotes cisplatin chemoresistance in MDA-MB-231 breast cancer derived cells through changes in gene expression and multiple signaling pathways.Biomedical reports · 2025Article
- Correction: Metformin inhibits the proliferation of benign prostatic epithelial cells.PloS one · 2023Article
- Systematic review of antitumour efficacy and mechanism of metformin activity in prostate cancer models.BJUI compass · 2023Review
- Metformin and Cancer Hallmarks: Molecular Mechanisms in Thyroid, Prostate and Head and Neck Cancer Models.Biomolecules · 2022Review
- Targeting Inflammatory Signaling in Prostate Cancer Castration Resistance.Journal of clinical medicine · 2021Review
- Metformin mitigates PLCε gene expression and modulates the Notch1/Hes and androgen receptor signaling pathways in castration-resistant prostate cancer xenograft models.Oncology letters · 2021Article
- Cell Adhesion Molecules in Plasticity and Metastasis.Molecular cancer research : MCR · 2021Review
- LCRF-0006, a small molecule mimetic of the N-cadherin antagonist peptide ADH-1, synergistically increases multiple myeloma response to bortezomib.FASEB bioAdvances · 2020Article
- Long Non-Coding RNA Plasmacytoma Variant Translocation 1 (PVT1) Enhances Proliferation, Migration, and Epithelial-Mesenchymal Transition (EMT) of Pituitary Adenoma Cells by Activating β-Catenin, c-Myc, and Cyclin D1 Expression.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Review
- N-cadherin in cancer metastasis, its emerging role in haematological malignancies and potential as a therapeutic target in cancer.BMC cancer · 2018Review
- Metformin: an antiproliferative agent and methylation regulator in treating prostatic disease?American journal of physiology. Renal physiology · 2018Article
- Metformin improves ovarian follicle dynamics by reducing theca cell proliferation and CYP-17 expression in an androgenized rat model.Journal of ovarian research · 2018Article
- Metformin Treatment Inhibits Motility and Invasion of Glioblastoma Cancer Cells.Analytical cellular pathology (Amsterdam) · 2018Article
- Blocking epithelial-to-mesenchymal transition in glioblastoma with a sextet of repurposed drugs: the EIS regimen.Oncotarget · 2017Article
- Probing the prostate tumour microenvironment II: Impact of hypoxia on a cell model of prostate cancer progression.Oncotarget · 2017Article
- Article
- T-cadherin in prostate cancer: relationship with cancer progression, differentiation and drug resistance.The journal of pathology. Clinical research · 2017Article
- Functional characterization of AMP-activated protein kinase signaling in tumorigenesis.Biochimica et biophysica acta · 2016Review
- Activation of AMPKα mediates additive effects of solamargine and metformin on suppressing MUC1 expression in castration-resistant prostate cancer cells.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Metformin has emerged as a potential anticancer agent. Here, we demonstrate that metformin plays an anti-tumor role via repressing N-cadherin, independent of AMPK, in wild-type N-cadherin cancer cells. Ectopic-expression of N-cadherin develops metformin-resistant cancer cells, while suppression of N-cadherin sensitizes cancer to metformin. Manipulation of AMPK expression does not alter sensitivity of cancer to metformin. We show that NF-kappaB is a downstream molecule of N-cadherin and metformin regulates NF-kappaB signaling via suppressing N-cadherin. Moreover, we also suggest that TWIST1 is an upstream molecule of N-cadherin/NF-kappaB signaling and manipulation of TWIST1 expression changes the sensitivity of cancer cells to metformin. In contrast to the cells that express N-cadherin, in N-cadherin deficient cells, metformin plays an anti-tumor role via activation of AMPK. Ectopic expression of N-cadherin makes cancer more resistant to metformin. Therefore, we suggest that metformin's anti-cancer therapeutic effect is mediated through different molecular mechanism in wild-type vs. deficient N-cadherin cancer cells. At last, we selected 49 out of 984 patients' samples with prostatic cancer after radical prostatectomy (selection criteria: Gleason score ≥ 7 and all patients taking metformin) and showed levels of N-cadherin, p65 and AMPK could predict post-surgical recurrence in prostate cancer after treatment of metformin.
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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.