ArticleBreast cancer research and treatment2018
The PPARγ agonist efatutazone delays invasive progression and induces differentiation of ductal carcinoma in situ.
Article in Breast cancer research and treatment, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- The adipokines in oral cancer pathogenesis and its potential as a new therapeutic approach.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- PPAR-γ in Melanoma and Immune Cells: Insights into Disease Pathogenesis and Therapeutic Implications.Cells · 2025Review
- Progression from ductal carcinoma in situ to invasive breast cancer: molecular features and clinical significance.Signal transduction and targeted therapy · 2024Review
- Targeting Adiponectin in Breast Cancer.Biomedicines · 2022Review
- An AIB1 Isoform Alters Enhancer Access and Enables Progression of Early-Stage Triple-Negative Breast Cancer.Cancer research · 2021Article
- Association of Adipose Tissue and Adipokines with Development of Obesity-Induced Liver Cancer.International journal of molecular sciences · 2021Review
- Breast cancer stem cells: A review of their characteristics and the agents that affect them.Molecular carcinogenesis · 2021Review
- PPAR-γ Modulators as Current and Potential Cancer Treatments.Frontiers in oncology · 2021Review
- Short- and Long-Term Effects of CDK4/6 Inhibition on Early-Stage Breast Cancer.Molecular cancer therapeutics · 2019Article
- Article
- In Vitro Models for Studying Invasive Transitions of Ductal Carcinoma In Situ.Journal of mammary gland biology and neoplasia · 2019Review
- Peroxisome proliferator-activated receptor gamma and BRCA1.Endocrine-related cancer · 2019Review
- Differential efatutazone's impact on mammary neoplasia dependent upon Brca1 dose.Endocrine-related cancer · 2018Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
purposeDuctal carcinoma in situ (DCIS) is a pre-invasive lesion of the breast considered a precursor of invasive ductal carcinoma. This study aimed to determine whether activated PPARγ acts as a tumor suppressor in human DCIS progression.
methodsWe utilized the high-affinity PPARγ agonist, efatutazone, to activate endogenous PPARγ in a well-defined model for the progression of basal (triple negative) DCIS, MCFDCIS cells, cultured under 2D and 3D conditions. We studied the effects of activated PPARγ on DCIS progression in MCFDCIS xenograft and C3(1)/Tag transgenic mice treated with 30 mg/kg of efatutazone.
resultsIn vitro, efatutazone did not alter the MCFDCIS cell proliferation but induced phenotypic and gene expression changes, indicating that activated PPARγ is able to differentiate MCFDCIS cells into more luminal and lactational-like cells. In addition, MCFDCIS tumorsphere formation in 3D was reduced by PPARγ activation. In vivo, efatutazone-treated MCFDCIS tumors exhibited fat deposition along with upregulation of PPARγ responsive genes in both epithelial and stromal compartments, suggesting features of milk-producing mammary epithelial cell differentiation. The efatutazone-treated lesions were less invasive with fewer CD44+/p63+ basal progenitor cells. PPARγ activation downregulated Akt phosphorylation in these tumors, although the ERK pathway remained unchanged. Similar trends in gene expression changes consistent with lactational and luminal cell differentiation were observed in the C3(1)/Tag mouse model after efatutazone treatment.
conclusionsOur data suggest that activation of the PPARγ pathway differentiates DCIS lesions and may be a useful approach to delay DCIS progression.
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