Abstract
C-C chemokine receptor 7 (CCR7) was one of the first two chemokine receptors that were found to be upregulated in breast cancers. Chemokine receptors promote chemotaxis of cells and tissue organization. Since under homeostatic conditions, CCR7 promotes migration of immune cells to lymph nodes, questions immediately arose regarding the ability of CCR7 to direct migration of cancer cells to lymph nodes. The literature since 2000 was examined to determine to what extent the expression of CCR7 in malignant tumors promoted migration to the lymph nodes. The data indicated that in different cancers, CCR7 plays distinct roles in directing cells to lymph nodes, the skin or to the central nervous system. In certain tumors, it may even serve a protective role. Future studies should focus on defining mechanisms that differentially regulate the unfavorable or beneficial role that CCR7 plays in cancer pathophysiology, to be able to improve outcomes in patients who harbor CCR7-positive cancers.
Highlights
C-C chemokine receptor 7 (CCR7) was the first lymphocyte-specific G protein-coupled receptor (GPCR) identified and was originally named Epstein–Barr virus (EBV)-induced gene 1 (EBI1) since it was upregulated in EBV-infected Burkitt’s lymphoma B cells [1]
CCR7 is a pivotal chemokine receptor for cell migration to secondary lymphoid organs, it is not surprising that tumor metastasis to lymph nodes was elevated when CCR7 expression was enhanced for all types of cancer
Actin dynamics are important for cell migration and at least for head and neck cancers and chronic leukemias, CCR7-activated actin filament accumulation at the cell membrane by stimulation of small GTPases, Ras homolog family member A (RhoA) and Cdc42, leading to lamellipodia, membrane ruffling and promotion of cell migration and invasive behavior [188,189,264,265]
Summary
C-C chemokine receptor 7 (CCR7) was the first lymphocyte-specific G protein-coupled receptor (GPCR) identified and was originally named Epstein–Barr virus (EBV)-induced gene 1 (EBI1) since it was upregulated in EBV-infected Burkitt’s lymphoma B cells [1]. Two ligands for CCR7 have been identified, CCL19 (MIP3β/ELC/CKβ11/EBI1-Ligand/SCYA19/exodus 3) [3–9] and CCL21(SLC/6ckine/SCYA21/exodus 2) [7,9–12] (Figure 1) These small polypeptides, 8 and 13 kDa, respectively, promote migration of CCR7-expressing activated dendritic cells and naïve T cells [3] to and within secondary lymphoid organs. The high levels of homology of mouse and human receptors and ligands make mouse models useful for studying CCR7 function relevant to cancer in humans. The high levels of mology of mouse and human receptors and ligands make mouse models useful for stu ying CCR7 function relevant to cancer in humans. Ous, transcellular chemokine gradients that induce cancer cell cThheemroolteasxiosftCoCdRra7ininincganlycmerpshaarteiccso[m31p]l.ex, and the reports are inconsistent. At times, this caOnubreurnedlaetresdtanbdacinkgtoofdhifofewretnucmesorisnuthsee cshceiemnotikfiicneasptporomaecthaesstatshiaztewtoedreifufesreedntotrislsauckes ogfaainpepdromporimateenctuomntrionl2s,00a0n,dwwhentrDyr.toAhnijaghMliügehltletrhaensed dDirf.feArlebnecretsZ. In our review, we discuss the reported clinical and animal study data and provide a summary of areas that are promising for further investigation
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