ArticleOncology letters2014
Regulation of insulin-like growth factor signaling by metformin in endometrial cancer cells.
Article in Oncology letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Do We Have Enough Evidence That Metformin Is Superior to Other Antidiabetic Drugs in Pancreatic Cancer Risk Reduction?International journal of molecular sciences · 2026Pooled it
- PRE-surgical Metformin In Uterine Malignancy (PREMIUM): a Multi-Center, Randomized Double-Blind, Placebo-Controlled Phase III Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Trial
- 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
- Synovial matrix turnover controls immune cell spatial patterning in inflammation resolution.Molecular systems biology · 2025Article
- Antitumor Effects of Metformin in Squamous Cell Carcinoma under Leptin Treatment Conditions.Preventive nutrition and food science · 2025Article
- Therapeutic Potential of Anti-Diabetes Drugs and Anti-Dyslipidemia Drugs to Mitigate Head and Neck Cancer Risk in Metabolic Syndrome.CNS neuroscience & therapeutics · 2025Review
- Metformin Impairs Linsitinib Anti-Tumor Effect on Ovarian Cancer Cell Lines.International journal of molecular sciences · 2024Article
- The impact of metformin on survival in diabetic endometrial cancer patients: a retrospective population-based analysis.Journal of diabetes and metabolic disorders · 2024Article
- Metformin Intervention-A Panacea for Cancer Treatment?Cancers · 2022Review
- Metformin for Cardiovascular Protection, Inflammatory Bowel Disease, Osteoporosis, Periodontitis, Polycystic Ovarian Syndrome, Neurodegeneration, Cancer, Inflammation and Senescence: What Is Next?ACS pharmacology & translational science · 2021Review
- Review
- IGFBP-1 in cancer: expression, molecular mechanisms, and potential clinical implications.American journal of translational research · 2021Review
- Changes in protein expression due to metformin treatment and hyperinsulinemia in a human endometrial cancer cell line.PloS one · 2021Article
- Therapeutic effect of metformin in the treatment of endometrial cancer.Oncology letters · 2020Review
- Endometrial Cancer as a Metabolic Disease with Dysregulated PI3K Signaling: Shedding Light on Novel Therapeutic Strategies.International journal of molecular sciences · 2020Review
- Benefits of Metformin in Attenuating the Hallmarks of Aging.Cell metabolism · 2020Review
- IGFBP-1 Expression Promotes Tamoxifen Resistance in Breast Cancer Cells via Erk Pathway Activation.Frontiers in endocrinology · 2020Article
- Glucose-dependent GPER1 expression modulates tamoxifen-induced IGFBP-1 accumulation.Journal of molecular endocrinology · 2019Article
- Metformin as a Therapeutic Target in Endometrial Cancers.Frontiers in oncology · 2018Review
- IGF-1 Receptor Modulates FoxO1-Mediated Tamoxifen Response in Breast Cancer Cells.Molecular cancer research : MCR · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity, diabetes and insulin resistance are marked risk factors that promote the development of type I endometrial cancer. Previous studies have demonstrated that insulin-like growth factor 1 (IGF-1) and IGF-2 promote cell proliferation in endometrial cancer cells, while metformin reverses this effect and inhibits cell proliferation. However, the effects of metformin on the regulation of the IGF signaling pathway are unclear. The aim of this study was to investigate the regulation of IGF signaling by metformin in endometrial cancer cells, and to determine the effects of metformin combined with IGF-1 receptor (IGF-1R) inhibitor on cell proliferation and apoptosis. Cell proliferation was assessed following exposure of Ishikawa and HEC-1B endometrial cancer cell lines to metformin and/or the IGF-1R inhibitor, PPP. Apoptosis was assessed by TdT-mediated dUTP nick end labeling assay. Metformin was observed to downregulate IGF-1R and upregulate IGF binding protein-1 (IGFBP-1) mRNA and protein expression, while compound C, an adenosine monophosphate protein kinase inhibitor, reversed this effect. Metformin administered with PPP inhibited endometrial cancer cell proliferation to a greater degree than treatment with either agent alone. At high concentrations (1 or 2 mM), metformin induced apoptosis in endometrial cancer cells. Metformin combined with IGF-1R axis inhibitors may act synergistically to kill tumor cells, as metformin was shown to delay and prevent IGF-1R feedback. In conclusion, this study supported the results of animal studies and subclinical studies, demonstrating the feasibility of metformin combined with IGF-1R axis inhibitors in the treatment of endometrial cancer.
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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.