ArticleBreast cancer research : BCR2019
Leptin produced by obesity-altered adipose stem cells promotes metastasis but not tumorigenesis of triple-negative breast cancer in orthotopic xenograft and patient-derived xenograft models.
Article in Breast cancer research : BCR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Genetic alterations inFrontiers in oncology · 2023Pooled it
- Closing the recapitulation gap in obesity-conditioned TNBC drug development.npj drug discovery · 2026Review
- NRG4 suppresses breast cancer metastasis via ERBB4-YAP1-mediated down-regulation of MMPs.Genes & diseases · 2026Article
- Obesity, Inflammation, and Tumor Microenvironment in Three-Dimensional Models of Breast Cancer.Cells · 2026Review
- Obesity-induced metabolic reprogramming of the tumor immune microenvironment: mechanisms, spatial niches, and immunotherapy response.Frontiers in immunology · 2026Review
- Bioinformatic Characterization of Genes That Are Correlated to the Progression of Breast Cancer to Breast Cancer Brain Metastasis.Cancer reports (Hoboken, N.J.) · 2025Article
- The correlation between obesity and the occurrence and development of breast cancer.European journal of medical research · 2025Review
- Peritoneal adipose stem cell-derived extracellular vesicles mediate the regulation of ovarian cancer cell proliferation and migration through EGFR-NF-κB signaling.Genes & diseases · 2025Article
- Significance of LIF/LIFR Signaling in the Progression of Obesity-Driven Triple-Negative Breast Cancer.Cancers · 2024Article
- Adipose Tissue in Breast Cancer Microphysiological Models to Capture Human Diversity in Preclinical Models.International journal of molecular sciences · 2024Review
- Obesity and lack of breastfeeding: a perfect storm to augment risk of breast cancer?Frontiers in oncology · 2024Review
- Liraglutide attenuates obese-associated breast cancer cell proliferation via inhibiting PI3K/Akt/mTOR signaling pathway.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024Article
- Obesity and leptin in breast cancer angiogenesis.Frontiers in endocrinology · 2024Review
- Fat Biology in Triple-Negative Breast Cancer: Immune Regulation, Fibrosis, and Senescence.Journal of obesity & metabolic syndrome · 2023Review
- Adipokines and epithelial-mesenchymal transition (EMT) in cancer.Molecular and cellular biochemistry · 2023Review
- Isoform-specific disruption of theeLife · 2023Article
- Obesity and cancer stem cells: Roles in cancer initiation, progression and therapy resistance.World journal of stem cells · 2023Review
- Targeting Breast Cancer Stem Cells.International journal of biological sciences · 2023Review
- The impact of obesity and adipokines on breast and gynecologic malignancies.Annals of the New York Academy of Sciences · 2022Review
- The effect of obesity on adipose-derived stromal cells and adipose tissue and their impact on cancer.Cancer metastasis reviews · 2022Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundBreast cancer is the second leading cause of cancer deaths in the USA. Triple-negative breast cancer (TNBC) is a clinically aggressive subtype of breast cancer with high rates of metastasis, tumor recurrence, and resistance to therapeutics. Obesity, defined by a high body mass index (BMI), is an established risk factor for breast cancer. Women with a high BMI have increased incidence and mortality of breast cancer; however, the mechanisms(s) by which obesity promotes tumor progression are not well understood.
methodsIn this study, obesity-altered adipose stem cells (obASCs) were used to evaluate obesity-mediated effects of TNBC. Both in vitro and in vivo analyses of TNBC cell lines were co-cultured with six pooled donors of obASCs (BMI > 30) or ASCs isolated from lean women (lnASCs) (BMI < 25).
resultsWe found that obASCs promote a pro-metastatic phenotype by upregulating genes associated with epithelial-to-mesenchymal transition and promoting migration in vitro. We confirmed our findings using a TNBC patient-derived xenograft (PDX) model. PDX tumors grown in the presence of obASCS in SCID/beige mice had increased circulating HLA1
conclusionsLeptin signaling is a potential mechanism through which obASCs promote metastasis of TNBC in both in vitro and in vivo analyses.
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Registered trials
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