期刊
CANCER RESEARCH
卷 80, 期 7, 页码 1475-1485出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-19-2961
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资金
- Howard Hughes Medical Institute
- NIH
- Breast Cancer Research Program (BCRP) Innovator Award from the Department of Defense office of the Congressionally Directed Medical Research Programs (CDMRP)
- Ludwig Center for Molecular Oncology at the Massachusetts Institute of Technology
- NIH Pre-Doctoral Training grant [T32GM007287]
- NCI Clinical Proteomic Tumor Analysis Consortium grants [NIH/NCI U24-CA210986, NIH/NCI U01 CA214125]
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. Significance: Tumor and stromal cells together create distinct ECM niches in breast cancer metastases to various tissues, providing new insight into how tumor cells adapt to survive in different tissue environments.
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