Cooperative and Escaping Mechanisms between Circulating Tumor Cells and Blood Constituents

• Published in: Cells (Basel, Switzerland) Vol. 8; no. 11; p. 1382
• Main Authors: Garrido-Navas, Carmen, de Miguel-Perez, Diego, Exposito-Hernandez, Jose, Bayarri, Clara, Amezcua, Victor, Ortigosa, Alba, Valdivia, Javier, Guerrero, Rosa, Garcia Puche, Jose Luis, Lorente, Jose Antonio, Serrano, Maria José
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 03.11.2019; MDPI
• Subjects: Apoptosis; Blood platelets; Cancer; circulating tumor cells; Cytokines; Extracellular matrix; Extravasation; Fibrin; Fibroblasts; Gene expression; Growth factors; Immune system; Immunotherapy; Inflammation; Kinases; Leukocytes (neutrophilic); Macrophages; Mesenchyme; Metabolites; Metastases; Metastasis; microbiome; Microbiomes; Microbiota; Myeloid cells; Natural killer cells; Neutrophils; Permeability; Phosphatase; Physiology; Platelets; Proteins; Review; tumor cell dissemination; Tumor cells; immune system; circulating tumor cells; microbiome; tumor cell dissemination
• ISSN: 2073-4409; 2073-4409
• DOI: 10.3390/cells8111382

Metastasis is the leading cause of cancer-related deaths and despite measurable progress in the field, underlying mechanisms are still not fully understood. Circulating tumor cells (CTCs) disseminate within the bloodstream, where most of them die due to the attack of the immune system. On the other hand, recent evidence shows active interactions between CTCs and platelets, myeloid cells, macrophages, neutrophils, and other hematopoietic cells that secrete immunosuppressive cytokines, which aid CTCs to evade the immune system and enable metastasis. Platelets, for instance, regulate inflammation, recruit neutrophils, and cause fibrin clots, which may protect CTCs from the attack of Natural Killer cells or macrophages and facilitate extravasation. Recently, a correlation between the commensal microbiota and the inflammatory/immune tone of the organism has been stablished. Thus, the microbiota may affect the development of cancer-promoting conditions. Furthermore, CTCs may suffer phenotypic changes, as those caused by the epithelial-mesenchymal transition, that also contribute to the immune escape and resistance to immunotherapy. In this review, we discuss the findings regarding the collaborative biological events among CTCs, immune cells, and microbiome associated to immune escape and metastatic progression.