ArticlePloS one2017
High Glucose-Mediated STAT3 Activation in Endometrial Cancer Is Inhibited by Metformin: Therapeutic Implications for Endometrial Cancer.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Prospective Randomized Biomarker Study of Metformin and Lifestyle Intervention for Prevention in Obese Women at Increased Risk for Endometrial Cancer.Cancer prevention research (Philadelphia, Pa.) · 2018Trial
- Obesity-driven extracellular vesicle signaling in cancer: mechanistic insights and clinical implications.Oncogenesis · 2026Review
- Metformin Impairs Linsitinib Anti-Tumor Effect on Ovarian Cancer Cell Lines.International journal of molecular sciences · 2024Article
- Article
- Review
- The role of ncRNAs and exosomes in the development and progression of endometrial cancer.Frontiers in oncology · 2024Review
- Article
- Insulin/IGF Axis and the Receptor for Advanced Glycation End Products: Role in Meta-inflammation and Potential in Cancer Therapy.Endocrine reviews · 2023Review
- Signal transducer and activator of transcription family is a prognostic marker associated with immune infiltration in endometrial cancer.Journal of clinical laboratory analysis · 2022Article
- Sera Protein Signatures of Endometrial Cancer Lymph Node Metastases.International journal of molecular sciences · 2022Article
- Effect of CMB Carrying PTX and CRISPR/Cas9 on Endometrial Cancer Naked Mouse Model.Journal of healthcare engineering · 2022Article
- Glucose Activates Lysine-Specific Demethylase 1 through the KEAP1/p62 Pathway.Antioxidants (Basel, Switzerland) · 2021Article
- Expression of the putative cannabinoid receptor GPR55 is increased in endometrial carcinoma.Histochemistry and cell biology · 2021Article
- High glucose: an emerging association between diabetes mellitus and cancer progression.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Preliminary evaluation on the beneficial effects of pioglitazone in the treatment of endometrial cancer.Medical oncology (Northwood, London, England) · 2021Article
- Article
- Correlation of Metabolic Factors with Endometrial Atypical Hyperplasia and Endometrial Cancer: Development and Assessment of a New Predictive Nomogram.Cancer management and research · 2021Article
- Mechanisms of JAK-STAT signaling pathway mediated by CXCL8 gene silencing on epithelial-mesenchymal transition of human cutaneous melanoma cells.Oncology letters · 2020Article
- Review
- Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
objectivesSTAT3 is over-expressed in endometrial cancer, and diabetes is a risk factor for the development of type 1 endometrial cancer. We therefore investigated whether glucose concentrations influence STAT3 expression in type 1 endometrial cancer, and whether such STAT3 expression might be inhibited by metformin.
methodsIn Ishikawa (grade 1) endometrial cancer cells subjected to media with low, normal, or high concentrations of glucose, expression of STAT3 and its target proteins was evaluated by real-time quantitative PCR (qPCR). Ishikawa cells were treated with metformin and assessed with cell proliferation, survival, migration, and ubiquitin assays, as well as Western blot and qPCR. Expression of apoptosis proteins was evaluated with Western blot in Ishikawa cells transfected with a STAT3 overexpression plasmid and treated with metformin. A xenograft tumor model was used for studying the in vivo efficacy of metformin.
resultsExpression of STAT3 and its target proteins was increased in Ishikawa cells cultured in high glucose media. In vitro, metformin inhibited cell proliferation, survival and migration but induced apoptosis. Metformin reduced expression levels of pSTAT3 ser727, total STAT3, and its associated cell survival and anti-apoptotic proteins. Additionally, metformin treatment was associated with increased degradation of pSTAT3 ser727. No change in apoptotic protein expression was noticed with STAT3 overexpression in Ishikawa cells. In vivo, metformin treatment led to a decrease in tumor weight as well as reductions of STAT3, pSTAT3 ser727, its target proteins.
conclusionsThese results suggest that STAT3 expression in type 1 endometrial cancer is stimulated by a high glucose environment and inhibited by metformin.
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