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The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues
Published on: June 16, 2018
Circulating Tumor Microparticles Promote Lung Metastasis by Reprogramming Inflammatory and Mechanical Niches via a
Huafeng Zhang1, Yuandong Yu1, Li Zhou1
1Department of Biochemistry and Molecular Biology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Abstract:
Despite the frequency of lung metastasis and its associated mortality, the mechanisms behind metastatic tumor cell survival and colonization in the lungs remain elusive. Here, we show that tumor cell-released microparticles (T-MPs) from the primary tumor site play a critical role in the metastatic process. The T-MPs remodeled the lung parenchyma via a macrophage-dependent pathway to create an altered inflammatory and mechanical response to tumor cell invasion. Mechanistically, we show that circulating T-MPs readily enter the lung parenchyma where they are taken up by local macrophages and induce CCL2 production. CCL2 recruits CD11b+Ly6Chigh inflammatory monocytes to the lungs where they mature into F4/80+CD11b+Ly6C- macrophages that not only produce IL6 but also trigger fibrin deposition. IL6 and the deposited fibrin facilitate the survival and growth of tumor-repopulating cells in the lungs by providing chemical and mechanical signals, respectively, thus setting the stage for lung metastasis. These data illustrate that T-MPs reprogram the lung microenvironment promoting metastasis. Cancer Immunol Res; 6(9); 1046-56. ©2018 AACR.
Insights
Tumor microparticles remodel the lung environment, promoting cancer metastasis. These particles recruit inflammatory cells that create conditions favoring tumor cell survival and growth in the lungs.
Area of Science:
- Oncology
- Immunology
- Cell Biology
Background:
- Lung metastasis is a frequent cause of cancer mortality, yet the mechanisms of tumor cell colonization remain unclear.
- Understanding how cancer cells survive and grow in the lungs is critical for developing effective treatments.
Purpose of the Study:
- To investigate the role of tumor cell-released microparticles (T-MPs) in establishing lung metastasis.
- To elucidate the cellular and molecular pathways by which T-MPs promote metastatic colonization.
Main Methods:
- Analysis of T-MPs' effects on lung parenchyma and immune cells.
- Investigating macrophage recruitment and activation by T-MPs.
- Assessing the roles of CCL2, IL6, and fibrin in supporting tumor cell survival.
Main Results:
- T-MPs from primary tumors remodel the lung microenvironment.
- T-MPs induce macrophages to produce CCL2, recruiting inflammatory monocytes.
- These monocytes mature into macrophages that produce IL6 and trigger fibrin deposition, aiding tumor cell survival and growth.
Conclusions:
- T-MPs reprogram the lung microenvironment to promote metastatic colonization.
- The T-MP-driven pathway involves macrophage activation, cytokine production, and fibrin deposition.
- Targeting T-MPs or their downstream effects could offer new strategies against lung metastasis.
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