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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Takano, Naoharu Semenza, Gregg L. Gilkes, Daniele M. Chaturvedi, Pallavi |
| Description | Author Affiliation: Chaturvedi P ( Vascular Program, Institute for Cell Engineering,McKusick-Nathans Institute of Genetic Medicine, and.); Gilkes DM ( Vascular Program, Institute for Cell Engineering,McKusick-Nathans Institute of Genetic Medicine, and.); Takano N ( Vascular Program, Institute for Cell Engineering,McKusick-Nathans Institute of Genetic Medicine, and.); Semenza GL ( Vascular Program, Institute for Cell Engineering,McKusick-Nathans Institute of Genetic Medicine, andDepartments of Pediatrics, Medicine, Oncology, Radiation Oncology, and Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205 gsemenza@jhmi.edu.); |
| Abstract | Intratumoral hypoxia induces the recruitment of stromal cells, such as macrophages and mesenchymal stem cells (MSCs), which stimulate invasion and metastasis by breast cancer cells (BCCs). Production of macrophage colony-stimulating factor 1 (CSF1) by BCCs is required for macrophage recruitment, but the mechanisms underlying CSF1 expression have not been delineated. Triple-negative breast cancers have increased expression of genes regulated by hypoxia-inducible factors (HIFs). In this study, we delineate two feed-forward signaling loops between human MDA-MB-231 triple-negative BCCs and human MSCs that drive stromal cell recruitment to primary breast tumors. The first loop, in which BCCs secrete chemokine (C-X-C motif) ligand 16 (CXCL16) that binds to C-X-C chemokine receptor type 6 (CXCR6) on MSCs and MSCs secrete chemokine CXCL10 that binds to receptor CXCR3 on BCCs, drives recruitment of MSCs. The second loop, in which MSCs secrete chemokine (C-C motif) ligand 5 that binds to C-C chemokine receptor type 5 on BCCs and BCCs secrete cytokine CSF1 that binds to the CSF1 receptor on MSCs, drives recruitment of tumor-associated macrophages and myeloid-derived suppressor cells. These two signaling loops operate independent of each other, but both are dependent on the transcriptional activity of HIFs, with hypoxia serving as a pathophysiological signal that synergizes with chemokine signals from MSCs to trigger CSF1 gene transcription in triple-negative BCCs. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 20 |
| Volume Number | 111 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2014-05-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Gene Expression Regulation, Neoplastic Hypoxia-Inducible Factor 1 Metabolism Macrophages Mesenchymal Stromal Cells Cytology Signal Transduction Triple Negative Breast Neoplasms Animals Bone Marrow Cells Cell Line, Tumor Cell Movement Chemokine CXCL10 Chemokines, CXC Gene Expression Profiling Anoxia Lung Neoplasms Lymphatic Metastasis Mammary Neoplasms, Experimental Mice Mice, Inbred BALB C Mice, SCID Neoplasm Transplantation Receptors, CCR5 Receptors, Scavenger Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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