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Adipose Cells Induce Escape from an Engineered Human Breast Microtumor Independently of their Obesity Status.

Authors
  • Dance, Yoseph W1
  • Obenreder, Mackenzie C1
  • Seibel, Alex J1
  • Meshulam, Tova2, 3
  • Ogony, Joshua W4
  • Lahiri, Nikhil1
  • Pacheco-Spann, Laura5
  • Radisky, Derek C4
  • Layne, Matthew D3
  • Farmer, Stephen R2, 3
  • Nelson, Celeste M6, 7
  • Tien, Joe1, 8
  • 1 Department of Biomedical Engineering, Boston University, 44 Cummington Mall, Boston, MA 02215 USA.
  • 2 Boston Nutrition Obesity Research Center, Boston University School of Medicine, Boston, MA USA.
  • 3 Department of Biochemistry, Boston University School of Medicine, Boston, MA USA.
  • 4 Department of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Jacksonville, FL USA.
  • 5 Department of Quantitative Health Sciences, Mayo Clinic Comprehensive Cancer Center, Jacksonville, FL USA.
  • 6 Department of Chemical and Biological Engineering, Princeton University, 303 Hoyt Laboratory, 25 William Street, Princeton, NJ 08544 USA.
  • 7 Department of Molecular Biology, Princeton University, Princeton, NJ USA.
  • 8 Division of Materials Science and Engineering, Boston University, Boston, MA USA.
Type
Published Article
Journal
Cellular and molecular bioengineering
Publication Date
Feb 01, 2023
Volume
16
Issue
1
Pages
23–39
Identifiers
DOI: 10.1007/s12195-022-00750-y
PMID: 36660589
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

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. 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. 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. 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. The online version contains supplementary material available at 10.1007/s12195-022-00750-y. © 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.

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