Adipose Cells Induce Escape from an Engineered Human Breast Microtumor Independently of their Obesity Status.
Autor: | Dance YW; Department of Biomedical Engineering, Boston University, 44 Cummington Mall, Boston, MA 02215 USA., Obenreder MC; Department of Biomedical Engineering, Boston University, 44 Cummington Mall, Boston, MA 02215 USA., Seibel AJ; Department of Biomedical Engineering, Boston University, 44 Cummington Mall, Boston, MA 02215 USA., Meshulam T; Boston Nutrition Obesity Research Center, Boston University School of Medicine, Boston, MA USA.; Department of Biochemistry, Boston University School of Medicine, Boston, MA USA., Ogony JW; Department of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Jacksonville, FL USA., Lahiri N; Department of Biomedical Engineering, Boston University, 44 Cummington Mall, Boston, MA 02215 USA., Pacheco-Spann L; Department of Quantitative Health Sciences, Mayo Clinic Comprehensive Cancer Center, Jacksonville, FL USA., Radisky DC; Department of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Jacksonville, FL USA., Layne MD; Department of Biochemistry, Boston University School of Medicine, Boston, MA USA., Farmer SR; Boston Nutrition Obesity Research Center, Boston University School of Medicine, Boston, MA USA.; Department of Biochemistry, Boston University School of Medicine, Boston, MA USA., Nelson CM; Department of Chemical and Biological Engineering, Princeton University, 303 Hoyt Laboratory, 25 William Street, Princeton, NJ 08544 USA.; Department of Molecular Biology, Princeton University, Princeton, NJ USA., Tien J; Department of Biomedical Engineering, Boston University, 44 Cummington Mall, Boston, MA 02215 USA.; Division of Materials Science and Engineering, Boston University, Boston, MA USA. |
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Jazyk: | angličtina |
Zdroj: | Cellular and molecular bioengineering [Cell Mol Bioeng] 2022 Dec 09; Vol. 16 (1), pp. 23-39. Date of Electronic Publication: 2022 Dec 09 (Print Publication: 2023). |
DOI: | 10.1007/s12195-022-00750-y |
Abstrakt: | Introduction: Obesity is associated with increased breast cancer incidence, recurrence, and mortality. Adipocytes and adipose-derived stem cells (ASCs), two resident cell types in adipose tissue, accelerate the early stages of breast cancer progression. It remains unclear whether obesity plays a role in the subsequent escape of malignant breast cancer cells into the local circulation. Methods: We engineered models of human breast tumors with adipose stroma that exhibited different obesity-specific alterations. We used these models to assess the invasion and escape of breast cancer cells into an empty, blind-ended cavity (as a mimic of a lymphatic vessel) for up to sixteen days. Results: Lean and obese donor-derived adipose stroma hastened escape to similar extents. Moreover, a hypertrophic adipose stroma did not affect the rate of adipose-induced escape. When admixed directly into the model tumors, lean and obese donor-derived ASCs hastened escape similarly. Conclusions: This study demonstrates that the presence of adipose cells, independently of the obesity status of the adipose tissue donor, hastens the escape of human breast cancer cells in multiple models of obesity-associated breast cancer. Supplementary Information: The online version contains supplementary material available at 10.1007/s12195-022-00750-y. Competing Interests: Conflict of interestYoseph W. Dance, Mackenzie C. Obenreder, Alex J. Seibel, Tova Meshulam, Joshua W. Ogony, Nikhil Lahiri, Laura Pacheco-Spann, Derek C. Radisky, Matthew D. Layne, Stephen R. Farmer, Celeste M. Nelson, and Joe Tien declare that they have no conflict of interest. (© The Author(s) under exclusive licence to Biomedical Engineering Society 2022, Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.) |
Databáze: | MEDLINE |
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