ArticleJournal of cellular and molecular medicine2018
Glyoxalase 1 sustains the metastatic phenotype of prostate cancer cells via EMT control.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 57 citations in OpenAlex.
- A comprehensive pan-cancer analysis of the prognostic role and immunotherapy efficacy evaluation of Glyoxalase 1.Discover oncology · 2025Article
- Acetylcholine Sustains LNCaP Prostate Cancer Cell Migration, Invasion and Proliferation Through Glyoxalase 1/MG-H1 Axis with the Involvement of Osteopontin.International journal of molecular sciences · 2025Article
- Glyoxalase 1 gene expression in various types of cancer cells immunopathology: a pan-cancer analysis study.Frontiers in oncology · 2025Article
- GLO1 regulates hepatocellular carcinoma proliferation and migration through the cell cycle pathway.BMC cancer · 2024Article
- Non-coding RNAs as potential targets in metformin therapy for cancer.Cancer cell international · 2024Review
- Review
- Molecular Assessment of Methylglyoxal-Induced Toxicity and Therapeutic Approaches in Various Diseases: Exploring the Interplay with the Glyoxalase System.Life (Basel, Switzerland) · 2024Review
- Dual Glyoxalase-1 and β-Klotho Gene-Activated Scaffold Reduces Methylglyoxal and Reprograms Diabetic Adipose-Derived Stem Cells: Prospects in Improved Wound Healing.Pharmaceutics · 2024Article
- EP300 as a Molecular Integrator of Fibrotic Transcriptional Programs.International journal of molecular sciences · 2023Review
- Systematic review of antitumour efficacy and mechanism of metformin activity in prostate cancer models.BJUI compass · 2023Review
- Differential gene expression and network analysis in head and neck squamous cell carcinoma.Molecular and cellular biochemistry · 2022Article
- Targeting Cancer Metabolism Plasticity with JX06 Nanoparticles via Inhibiting PDK1 Combined with Metformin for Endometrial Cancer Patients with Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Regulation of Neuroendocrine-like Differentiation in Prostate Cancer by Non-Coding RNAs.Non-coding RNA · 2021Review
- Metastatic Prostate Cancer Cells Secrete Methylglyoxal-Derived MG-H1 to Reprogram Human Osteoblasts into a Dedifferentiated, Malignant-like Phenotype: A Possible Novel Player in Prostate Cancer Bone Metastases.International journal of molecular sciences · 2021Article
- Glyoxal-Lysine Dimer, an Advanced Glycation End Product, Induces Oxidative Damage and Inflammatory Response by Interacting with RAGE.Antioxidants (Basel, Switzerland) · 2021Article
- Glyoxalase 1 Expression as a Novel Diagnostic Marker of High-Grade Prostatic Intraepithelial Neoplasia in Prostate Cancer.Cancers · 2021Article
- Article
- Methylglyoxal-Dependent Glycative Stress Is Prevented by the Natural Antioxidant Oleuropein in Human Dental Pulp Stem Cells through Nrf2/Glo1 Pathway.Antioxidants (Basel, Switzerland) · 2021Article
- Article
- Biochemical Regulation of the Glyoxalase System in Response to Insulin Signaling.Antioxidants (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastasis is the primary cause of death in prostate cancer (PCa) patients. Effective therapeutic intervention in metastatic PCa is undermined by our poor understanding of its molecular aetiology. Defining the mechanisms underlying PCa metastasis may lead to insights into how to decrease morbidity and mortality in this disease. Glyoxalase 1 (Glo1) is the detoxification enzyme of methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs). Hydroimidazolone (MG-H1) and argpyrimidine (AP) are AGEs originating from MG-mediated post-translational modification of proteins at arginine residues. AP is involved in the control of epithelial to mesenchymal transition (EMT), a crucial determinant of cancer metastasis and invasion, whose regulation mechanisms in malignant cells are still emerging. Here, we uncover a novel mechanism linking Glo1 to the maintenance of the metastatic phenotype of PCa cells by controlling EMT by engaging the tumour suppressor miR-101, MG-H1-AP and TGF-β1/Smad signalling. Moreover, circulating levels of Glo1, miR-101, MG-H1-AP and TGF-β1 in patients with metastatic compared with non-metastatic PCa support our in vitro results, demonstrating their clinical relevance. We suggest that Glo1, together with miR-101, might be potential therapeutic targets for metastatic PCa, possibly by metformin administration.
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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 Socratic graph.