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Proteomic Profiling of the ECM of Xenograft Breast Cancer Metastases in Different Organs Reveals Distinct Metastatic Niches
Name
nihms-1558781.pdf
Description
Accepted version
Size
2 MB
Format
Adobe PDF
Checksum (MD5)
c529825b9b7651e69b62fb713721dc78
Author(s)
Hebert, Jess D
Myers, Samuel A
Naba, Alexandra
Abbruzzese, Genevieve
Lamar, John M
Carr, Steven A
Hynes, Richard O
Date Issued
2020
Journal
Cancer Research
Publisher
American Association for Cancer Research (AACR)
Version
Author's final manuscript
Abstract
© 2020 American Association for Cancer Research. Metastasis causes most cancer-related deaths, and one poorly understood aspect of metastatic cancer is the adaptability of cells from a primary tumor to create new niches and survive in multiple, different secondary sites. We used quantitative mass spectrometry to analyze the extracellular matrix (ECM), a critical component of metastatic niches, in metastases to the brain, lungs, liver, and bone marrow, all derived from parental MDA-MB-231 triple-negative breast cancer cells. Tumor and stromal cells cooperated in forming niches; stromal cells produced predominantly core, structural ECM proteins and tumor cells produced a diverse array of ECM-associated proteins, including secreted factors and modulators of the matrix. In addition, tumor and stromal cells together created distinct niches in each tissue. Downregulation of SERPINB1, a protein elevated in brain metastases, led to a reduction in brain metastasis, suggesting that some niche-specific ECM proteins may be involved in metastatic tropism.
Terms of Use
Creative Commons Attribution-Noncommercial-Share Alike
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DOI of Published Version
10.1158/0008-5472.CAN-19-2961
