Here is a great survey paper talking about all the
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Posted On: 09/24/2020 12:48:06 AM
Here is a great survey paper talking about all the points we raised last year.
The CCL5/CCR5 Axis in Cancer Progression
Donatella Aldinucci * , Cinzia Borghese and Naike Casagrande
https://res.mdpi.com/d_attachment/cancers/can...-01765.pdf
Figure 1. Involvement of the CCL5/CCR5 axis in cancer progression. (1) CCL5, secreted by tumor cells (autocrine) and by the TME (paracrine), increases tumor growth. (2) CCL5 induces collagen degradation by activating matrix metalloproteinases in macrophages and fibroblasts. (3) CCL5 increases tumor cell migration and invasion by integrin activation (adhesion) and actin polarization. (4) CCR5+ cancer cells show characteristics of cancer stem cells. (5) CCR5 expression associates with stronger repair responses to DNA damage induced by doxorubicin and γ-irradiation. (6) CCL5 secreted by tumor cells and by the TME decreases drug cytotoxic activity. (7) CCR5 engagement stimulates glucose uptake, glycolysis, pentose phosphate pathway, fatty acid synthesis, and glutamine metabolism. (
CCL5 promotes endothelial cell migration and neovessel formation, and induces the secretion of VEGF by endothelial cells. (9) CCL5 secreted by tumor cells recruits normal cells to build the TME. (10) CCL5 induces the immunosuppressive polarization of monocytes and myeloid cells leading to M2-TAMs and MDSCs that induce exhaustion of effector T-cells. Protein kinase B, Akt; cancer-associated fibroblast, CAF; C-C chemokine ligand 5, CCL5; C-C chemokine receptor type 5, CCR5; cancer stem cell, CSC; extracellular matrix, ECM; extracellular signal-regulated kinase, ERK; janus kinase, JAK; mitogen-activated protein kinase, MAPK; matrix metalloproteinase, MMP; myeloid-derived suppressor cell, MDSC; mesenchymal stem cell, MSC; nuclear factor kappa-light-chain-enhancer of activated B cells, NF-kB; phosphoinositide-3-kinase, PI3K; signal transducer and activator of transcription protein, STAT3; tumor-associated macrophage, TAM; tumor microenvironment, TME; regulatory T cell, Treg; vascular endothelial growth factor, VEGF.
The CCL5/CCR5 Axis in Cancer Progression
Donatella Aldinucci * , Cinzia Borghese and Naike Casagrande
https://res.mdpi.com/d_attachment/cancers/can...-01765.pdf
Figure 1. Involvement of the CCL5/CCR5 axis in cancer progression. (1) CCL5, secreted by tumor cells (autocrine) and by the TME (paracrine), increases tumor growth. (2) CCL5 induces collagen degradation by activating matrix metalloproteinases in macrophages and fibroblasts. (3) CCL5 increases tumor cell migration and invasion by integrin activation (adhesion) and actin polarization. (4) CCR5+ cancer cells show characteristics of cancer stem cells. (5) CCR5 expression associates with stronger repair responses to DNA damage induced by doxorubicin and γ-irradiation. (6) CCL5 secreted by tumor cells and by the TME decreases drug cytotoxic activity. (7) CCR5 engagement stimulates glucose uptake, glycolysis, pentose phosphate pathway, fatty acid synthesis, and glutamine metabolism. (
CCL5 promotes endothelial cell migration and neovessel formation, and induces the secretion of VEGF by endothelial cells. (9) CCL5 secreted by tumor cells recruits normal cells to build the TME. (10) CCL5 induces the immunosuppressive polarization of monocytes and myeloid cells leading to M2-TAMs and MDSCs that induce exhaustion of effector T-cells. Protein kinase B, Akt; cancer-associated fibroblast, CAF; C-C chemokine ligand 5, CCL5; C-C chemokine receptor type 5, CCR5; cancer stem cell, CSC; extracellular matrix, ECM; extracellular signal-regulated kinase, ERK; janus kinase, JAK; mitogen-activated protein kinase, MAPK; matrix metalloproteinase, MMP; myeloid-derived suppressor cell, MDSC; mesenchymal stem cell, MSC; nuclear factor kappa-light-chain-enhancer of activated B cells, NF-kB; phosphoinositide-3-kinase, PI3K; signal transducer and activator of transcription protein, STAT3; tumor-associated macrophage, TAM; tumor microenvironment, TME; regulatory T cell, Treg; vascular endothelial growth factor, VEGF. 
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