ArticleThe American journal of pathology2011
In vivo and in vitro evidence that PPARγ ligands are antagonists of leptin signaling in breast cancer.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Leptin signaling in breast cancer and its crosstalk with peroxisome proliferator-activated receptors α and γ.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Pooled it
- Bidirectional regulation of lipid metabolism and the tumor microenvironment: new perspectives from mechanism to therapy.Frontiers in immunology · 2025Review
- Pioglitazone enhances cisplatin's impact on triple-negative breast cancer: Role of PPARγ in cell apoptosis.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024Article
- Obesity-Associated Breast Cancer: Analysis of Risk Factors and Current Clinical Evaluation.Advances in experimental medicine and biology · 2024Review
- Lipid metabolism reprogramming in tumor-associated macrophages and implications for therapy.Lipids in health and disease · 2023Review
- The Role of PPARs in Breast Cancer.Cells · 2022Review
- Targeting Adiponectin in Breast Cancer.Biomedicines · 2022Review
- Review
- Review
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- Estrogen Sulfotransferase is Highly Expressed in Vascular Endothelial Cells Overlying Atherosclerotic Plaques.The protein journal · 2022Article
- Nutraceuticals in the Mediterranean Diet: Potential Avenues for Breast Cancer Treatment.Nutrients · 2021Review
- PPARgamma: A Potential Intrinsic and Extrinsic Molecular Target for Breast Cancer Therapy.Biomedicines · 2021Article
- Association of Adipose Tissue and Adipokines with Development of Obesity-Induced Liver Cancer.International journal of molecular sciences · 2021Review
- miR-22-3p/PGC1PPAR research · 2021Article
- The Adipokine Component in the Molecular Regulation of Cancer Cell Survival, Proliferation and Metastasis.Pathology oncology research : POR · 2021Review
- Natural and Synthetic PPARγ Ligands in Tumor Microenvironment: A New Potential Strategy against Breast Cancer.International journal of molecular sciences · 2020Review
- Review
- Cytoplasmic PPARγ is a marker of poor prognosis in patients with Cox-1 negative primary breast cancers.Journal of translational medicine · 2020Article
- Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity is a major risk factor for the development and progression of breast cancer. Leptin, a cytokine mainly produced by adipocytes, plays a crucial role in mammary carcinogenesis and is elevated in hyperinsulinemia and insulin resistance. The antidiabetic thiazolidinediones inhibit leptin gene expression through ligand activation of the peroxisome proliferator-activated receptor-γ (PPARγ) and exert antiproliferative and apoptotic effects on breast carcinoma. In this study, we investigated the ability of PPARγ ligands to counteract leptin stimulatory effects on breast cancer growth in either in vivo or in vitro models. The results show that activation of PPARγ prevented the development of leptin-induced MCF-7 tumor xenografts and inhibited the increased cell-cell aggregation and proliferation observed on leptin exposure. PPARγ ligands abrogated the leptin-induced up-regulation of leptin gene expression and its receptors in breast cancer. PPARγ-mediated repression of leptin gene involved the recruitment of nuclear receptor corepressor protein and silencing mediator of retinoid and thyroid hormone receptors corepressors on the glucocorticoid responsive element site in the leptin gene expression regulatory region in the presence of glucocorticoid receptor and PPARγ. In addition, PPARγ ligands inhibited leptin signaling mediated by MAPK/STAT3/Akt phosphorylation and counteracted leptin stimulatory effect on estrogen signaling. These findings suggest that PPARγ ligands may have potential therapeutic benefits in the treatment of breast cancer.
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