We saw pro 140 and RANTES(regulated on activation, normal T cell expressed and secrete) act very nice similarly in the last paper posted, more so than other ccr5 antagonists like maraviroc. More rantes papers, pro 140 can inhibit this interaction between rantes and ccr5, probably by competition binding at similar locations, which is a large part of why it is working in so many indications: cancer cell movement, inflammatory diseases, etc.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC...035101.pdf
Now widely established as an inflammatory chemokine, CCL5 is known to mediate chemotactic activity in T cells, monocytes, dendritic cells, natural killer cells, eosinophils, and basophils [2,3,4]. CCL5 is associated with chronic inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease, and cancer [5,6]. An association between CCL5 expression and cancer has been reported in melanoma, lung, prostate, and pancreatic cancers [7,8,9]. The most striking findings thus far have been with breast cancer [7,8]. Several investigations have reported that CCL5 was detected in samples from patients with breast cancer and that expression levels correlated with disease progression [7,8].
CCL5 has been reported to stimulate directional migration and invasion of human cancer cells [23,30]. CCL5-trigered migration in osteosarcoma cells was examined using the Transwell assay. CCL5 directed human osteosarcoma cell migration (U2OS and MG63 cells) (Fig. 1A). We also found that CCL5 increased invasive ability of human osteosarcoma cells through Matrigel basement membrane matrix (Fig. 1B). Interaction of CCL5 with its specific receptor CCR on the surface of cancer cells has been reported to induce cancer migration [7,22]. Stimulation of cells with CCL5 increased the mRNA expression of CCR5 but not CCR1 and CCR3 (Fig. 1C), suggesting that the amplification loop strengthens the CCL5-CCR5-signaling pathway. Pretreatment of cells with CCR5 mAb or CCR5 receptor inhibitor (Met- RANTES) reduced CCL5-increaed cell migration (Fig. 1D). In addition, transfection of cells with CCR5 siRNA also blocked CCL5-induced cell migration activity (Fig. 1E). Therefore, CCL5 and CCR5 interaction is very important in migration activity of osteosarcoma cells.
https://cancerres.aacrjournals.org/content/65...ent/1108.2
Expression of the prototypic inflammatory chemokine CCL5 (RANTES) by tumor cells is thought to correlate with the progression of several cancers, through the recruitment of inflammatory leukocytes. Furthermore, CCL5 was shown to induce breast cancer cell migration, mediated by the receptor CCR5
https://www.ncbi.nlm.nih.gov/pubmed/17641205
CCR1/CCL5 (RANTES) receptor-ligand interactions modulate allogeneic T-cell responses and graft-versus-host disease following stem-cell transplantation.
https://www.nature.com/articles/s41598-018-25699-9
Our data indicate that chemokine Ccl5 is one of the HSC-secreted mediators in early NASH in humans and in mice fed with choline-deficient, L-amino acid defined, high fat diet. Furthermore, Ccl5 directly induces steatosis and pro-inflammatory factors in healthy hepatocytes through the receptor Ccr5.
2001 paper
The CC chemokine RANTES as a potential contributor to breast cancer progression
https://breast-cancer-research.biomedcentral....186/bcr377
2002 paper
RANTES Expression Is a Predictor of Survival in Stage I Lung Adenocarcinoma
https://clincancerres.aacrjournals.org/conten...3.full.pdf
https://www.hindawi.com/journals/omcl/2014/208408/
Correlation between Serum RANTES Levels and the Severity of Parkinson’s Disease
Example
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC...035101.pdf
Now widely established as an inflammatory chemokine, CCL5 is known to mediate chemotactic activity in T cells, monocytes, dendritic cells, natural killer cells, eosinophils, and basophils [2,3,4]. CCL5 is associated with chronic inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease, and cancer [5,6]. An association between CCL5 expression and cancer has been reported in melanoma, lung, prostate, and pancreatic cancers [7,8,9]. The most striking findings thus far have been with breast cancer [7,8]. Several investigations have reported that CCL5 was detected in samples from patients with breast cancer and that expression levels correlated with disease progression [7,8].
CCL5 has been reported to stimulate directional migration and invasion of human cancer cells [23,30]. CCL5-trigered migration in osteosarcoma cells was examined using the Transwell assay. CCL5 directed human osteosarcoma cell migration (U2OS and MG63 cells) (Fig. 1A). We also found that CCL5 increased invasive ability of human osteosarcoma cells through Matrigel basement membrane matrix (Fig. 1B). Interaction of CCL5 with its specific receptor CCR on the surface of cancer cells has been reported to induce cancer migration [7,22]. Stimulation of cells with CCL5 increased the mRNA expression of CCR5 but not CCR1 and CCR3 (Fig. 1C), suggesting that the amplification loop strengthens the CCL5-CCR5-signaling pathway. Pretreatment of cells with CCR5 mAb or CCR5 receptor inhibitor (Met- RANTES) reduced CCL5-increaed cell migration (Fig. 1D). In addition, transfection of cells with CCR5 siRNA also blocked CCL5-induced cell migration activity (Fig. 1E). Therefore, CCL5 and CCR5 interaction is very important in migration activity of osteosarcoma cells.
https://cancerres.aacrjournals.org/content/65...ent/1108.2
Expression of the prototypic inflammatory chemokine CCL5 (RANTES) by tumor cells is thought to correlate with the progression of several cancers, through the recruitment of inflammatory leukocytes. Furthermore, CCL5 was shown to induce breast cancer cell migration, mediated by the receptor CCR5
https://www.ncbi.nlm.nih.gov/pubmed/17641205
CCR1/CCL5 (RANTES) receptor-ligand interactions modulate allogeneic T-cell responses and graft-versus-host disease following stem-cell transplantation.
https://www.nature.com/articles/s41598-018-25699-9
Our data indicate that chemokine Ccl5 is one of the HSC-secreted mediators in early NASH in humans and in mice fed with choline-deficient, L-amino acid defined, high fat diet. Furthermore, Ccl5 directly induces steatosis and pro-inflammatory factors in healthy hepatocytes through the receptor Ccr5.
2001 paper
The CC chemokine RANTES as a potential contributor to breast cancer progression
https://breast-cancer-research.biomedcentral....186/bcr377
2002 paper
RANTES Expression Is a Predictor of Survival in Stage I Lung Adenocarcinoma
https://clincancerres.aacrjournals.org/conten...3.full.pdf
https://www.hindawi.com/journals/omcl/2014/208408/
Correlation between Serum RANTES Levels and the Severity of Parkinson’s Disease
Example
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