ArticleInternational journal of cancer2014
Loss of PPARγ expression in mammary secretory epithelial cells creates a pro-breast tumorigenic environment.
Article in International journal of cancer, 2014. 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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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, 42 citations in OpenAlex.
- Article
- Prenatal airborne polycyclic aromatic hydrocarbon exposure, altered regulation of peroxisome proliferator-activated receptor gamma (Ppar)γ, and links with mammary cancer.Environmental research · 2023Article
- Changes in the mammary gland during aging and its links with breast diseases.Acta biochimica et biophysica Sinica · 2023Review
- Review
- Comparative and analytical characterization of the oral bacteriome of smokeless tobacco users with oral squamous cell carcinoma.Applied microbiology and biotechnology · 2022Article
- Identification of Crucial lncRNAs for Luminal A Breast Cancer through RNA Sequencing.International journal of endocrinology · 2022Article
- Study on the effects of the different polar group of EPA-enriched phospholipids on the proliferation and apoptosis in 95D cells.Marine life science & technology · 2021Article
- Inflammation and tumor progression: signaling pathways and targeted intervention.Signal transduction and targeted therapy · 2021Article
- Endurance Exercise Mitigates Immunometabolic Adipose Tissue Disturbances in Cancer and Obesity.International journal of molecular sciences · 2020Review
- The Importance of Breast Adipose Tissue in Breast Cancer.International journal of molecular sciences · 2020Review
- Effects of Maternal Grape Juice Intake on Unfolded Protein Response in the Mammary Glands of Offspring of High Fat Diet Fed Rat Dams.Nutrients · 2020Article
- Heightened susceptibility: A review of how pregnancy and chemical exposures influence maternal health.Reproductive toxicology (Elmsford, N.Y.) · 2020Review
- MLAA-34 knockdown shows enhanced antitumor activity via JAK2/STAT3 signaling pathway in acute monocytic leukemia.Journal of Cancer · 2020Article
- Review
- Paternal malnutrition programs breast cancer risk and tumor metabolism in offspring.Breast cancer research : BCR · 2018Article
- Integrated bioinformatics analysis reveals key candidate genes and pathways in breast cancer.Molecular medicine reports · 2018Article
- Mammary alveolar epithelial cells convert to brown adipocytes in post-lactating mice.Journal of cellular physiology · 2017Article
- Social isolation induces autophagy in the mouse mammary gland: link to increased mammary cancer risk.Endocrine-related cancer · 2016Article
- Biological underpinnings of breastfeeding challenges: the role of genetics, diet, and environment on lactation physiology.American journal of physiology. Endocrinology and metabolism · 2016Review
- Paternal overweight is associated with increased breast cancer risk in daughters in a mouse model.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Breast cancer is the leading cause of new cancer diagnoses among women. Using peroxisome proliferator-activated receptor (PPAR)γ((+/-)) mice, we showed normal expression of PPARγ was critical to stop 7,12-dimethylbenz[a]anthracene (DMBA)-induced breast tumorigenesis. PPARγ is expressed in many breast cell types including mammary secretory epithelial (MSE) cells. MSEs proliferate as required during pregnancy, and undergo apoptosis or reversible transdifferentiation during involution once lactation is complete. Thus, MSE-specific loss of PPARγ was hypothesized to enhance DMBA-mediated breast tumorigenesis. To test this, MSE cell-specific PPARγ knockout (PPARγ-MSE KO) and control (PPARγ-WT) mice were generated, mated and allowed to nurse for three days. One week after involution, dams were treated with DMBA to initiate breast tumors, and randomized on week 7 to continue receiving a normal chow diet (DMBA Only: PPARγ-WT, n = 15; PPARγ-MSE KO, n = 25) or one supplemented with a PPARγ activating drug (DMBA + ROSI: PPARγ-WT, n = 17; PPARγ-MSE KO, n = 24), and monitored for changes in breast tumor outcomes. PPARγ-MSE KOs had significantly lower overall survival and decreased mammary tumor latency as compared to PPARγ-WT controls. PPARγ activation significantly reduced DMBA-mediated malignant mammary tumor volumes irrespective of genotype. MSE-specific PPARγ loss resulted in decreased mammary gland expression of PTEN and Bax, increased superoxide anion production, and elevated serum eotaxin and RANTES, creating a protumorigenic environment. Moreover, PPARγ activation in MSEs delayed mammary tumor growth in part by down-regulating Cox-1, Cox-2 and cyclin D1. Collectively, these studies highlight a protective role of MSE-specific PPARγ during breast tumorigenesis, and support a novel chemotherapeutic role of PPARγ activation in breast cancer.
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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.