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CCL2 in the tumor microenvironment.

In: Tumor Microenvironment. New York: Springer, 2021. 1-14 (Adv. Exp. Med. Biol. ; 1302)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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.
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Publikationstyp Artikel: Sammelbandbeitrag/Buchkapitel
Korrespondenzautor
Schlagwörter Angiogenesis ; Ccl2 ; Ccr2 ; Cancer ; Extravasation ; Immunity ; Immunosuppression ; Invasion ; Mcp-1 ; Macrophage ; Metastasis ; Microenvironment ; Nfκb ; Tam ; Tumor; Monocyte Chemoattractant Protein-1; Chemokine Receptor Ccr2; Foster Immune Privilege; Macrophage Infiltration; Chemotactic Protein-1; Breast-cancer; Cell-migration; Functional Expression; Molecular-cloning; Transendothelial Migration
ISSN (print) / ISBN 0065-2598
Bandtitel Tumor Microenvironment
Quellenangaben Band: 1302, Heft: , Seiten: 1-14 Artikelnummer: , Supplement: ,
Verlag Springer
Verlagsort New York
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed