ReviewJournal of cellular and molecular medicine
PPARgamma activation by thiazolidinediones (TZDs) may modulate breast carcinoma outcome: the importance of interplay with TGFbeta signalling.
Review in Journal of cellular and molecular medicine. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
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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
24 citing papers in PubMed, 49 citations in OpenAlex.
- Thiazolidinedione derivatives in cancer therapy: exploring novel mechanisms, therapeutic potentials, and future horizons in oncology.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Design, Synthesis and Biological Evaluation of Thiazolidine-2,4-dione-biphenyl Derivatives as Anticancer Agents.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Green synthesis,RSC advances · 2024Article
- PPARγ Acetylation in Adipocytes Exacerbates BAT Whitening and Worsens Age-Associated Metabolic Dysfunction.Cells · 2023Article
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- Article
- PPARα-Selective Antagonist GW6471 Inhibits Cell Growth in Breast Cancer Stem Cells Inducing Energy Imbalance and Metabolic Stress.Biomedicines · 2021Article
- Glitazone loaded fat enhances adiponectin production and inhibits breast cancer cell proliferation.Molecular biology reports · 2019Article
- Differential characterization of myogenic satellite cells with linolenic and retinoic acid in the presence of thiazolidinediones from prepubertal Korean black goats.Asian-Australasian journal of animal sciences · 2018Article
- Evaluation of Antioxidant Intakes in Relation to Inflammatory Markers Expression Within the Normal Breast Tissue of Breast Cancer Patients.Integrative cancer therapies · 2017Article
- Ligand-activated PPARγ downregulates CXCR4 gene expression through a novel identified PPAR response element and inhibits breast cancer progression.Oncotarget · 2016Article
- Lipid-sensors, enigmatic-orphan and orphan nuclear receptors as therapeutic targets in breast-cancer.Oncotarget · 2016Review
- PPARγ Agonists as an Anti-Inflammatory Treatment Inhibiting Rotavirus Infection of Small Intestinal Villi.PPAR research · 2016Article
- Dietary tocopherols inhibit cell proliferation, regulate expression of ERα, PPARγ, and Nrf2, and decrease serum inflammatory markers during the development of mammary hyperplasia.Molecular carcinogenesis · 2013Article
- Chemopreventive activity of vitamin E in breast cancer: a focus on γ- and δ-tocopherol.Nutrients · 2011Review
- Specific thiazolidinediones inhibit ovarian cancer cell line proliferation and cause cell cycle arrest in a PPARγ independent manner.PloS one · 2011Article
- Troglitazone suppresses telomerase activity independently of PPARgamma in estrogen-receptor negative breast cancer cells.BMC cancer · 2010Article
- Insulin-sensitizing therapy attenuates type 2 diabetes-mediated mammary tumor progression.Diabetes · 2010Article
- Article
- A Role for the PPARgamma in Cancer Therapy.PPAR research · 2008Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The thiazolidinediones (TZDs) are a class of synthetic antidiabetic drugs exerting its action primarily upon activation of the peroxisome proliferator-activated receptor-gamma (PPARgamma). Given the widespread incidence of diabetes type II and lifelong exposure of these patients to TZDs, there is a possibility that chronic treatment with TZD modifies clinical phenotypes of other common human diseases, for example breast carcinoma. There is evidence that TZDs act as breast carcinoma suppression agents, at least in the in vitro and animal models. Stimulation of the PPARgamma by TZDs interferes with oestrogen receptor signalling, STAT5B and NF-kappaB signalling cascades. On the other hand, TZDs repress TGFbeta signalling, a well-known suppressor of the initial stages of breast carcinoma development. Another layer of complexity arises at the later stages of tumour development, when TGFbeta acts as a tumour promoter: its overexpression is associated with poor prognosis, higher degree of tumour vascularization and metastasis. Longitudinal studies of breast carcinoma development in chronic TZD users are needed. In this review, we dissect possible interplays between chronic exposure of breast tis-sue to TZDs and TGFbeta signalling and predict influence of TZD exposure on cancer-related clinical outcome.
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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.