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| Book/Journal Article | DKFZ-2021-01638 |
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2021
Springer
[Heidelberg]
ISBN: 978-3-030-62657-0 (print), 978-3-030-62658-7 (electronic)
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Please use a persistent id in citations: doi:doi: 10.1007/978-3-030-62658-7_1 doi:10.1007/978-3-030-62658-7_1
Abstract: The C-C motif chemokine ligand 2 (CCL2) is a crucial mediator of immune cell recruitment during microbial infections and tissue damage. CCL2 is also frequently overexpressed in cancer cells and other cells in the tumor microenvironment, and a large body of evidence indicates that high CCL2 levels are associated with more aggressive malignancies, a higher probability of metastasis, and poorer outcomes in a wide range of cancers. CCL2 plays a role in recruiting tumor-associated macrophages (TAMs), which adopt a pro-tumorigenic phenotype and support cancer cell survival, facilitate tumor cell invasion, and promote angiogenesis. CCL2 also has direct, TAM-independent effects on tumor cells and the tumor microenvironment, including recruitment of other myeloid subsets and non-myeloid cells, maintaining an immunosuppressive environment, stimulating tumor cell growth and motility, and promoting angiogenesis. CCL2 also plays important roles in the metastatic cascade, such as creating a pre-metastatic niche in distant organs and promoting tumor cell extravasation across endothelia. Due to its many roles in tumorigenesis and metastatic processes, the CCL2-CCR2 signaling axis is currently being pursued as a potential therapeutic target for cancer.
Keyword(s): Cell Line, Tumor (MeSH) ; Chemokine CCL2: genetics (MeSH) ; Chemokines (MeSH) ; Ligands (MeSH) ; Receptors, CCR2: genetics (MeSH) ; Tumor Microenvironment (MeSH) ; Angiogenesis ; CCL2 ; CCR2 ; Cancer ; Extravasation ; Immunity ; Immunosuppression ; Invasion ; MCP-1 ; Macrophage ; Metastasis ; Microenvironment ; NFκB ; TAM ; Tumor ; Chemokine CCL2 ; Chemokines ; Ligands ; Receptors, CCR2
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