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The secretion of CCL5 and CCL2 was stimulated in undifferentiated and decidualized ESCs by the combination of TNF-alpha and IFN-gamma under non-apoptotic as well as apoptotic (with Fas-stimulation in parallel) conditions. TNF-alpha or IFN-gamma alone did not have this effect. The stimulatory influence of TNF-alpha plus IFN-gamma on CCL5 and CCL2 in ESCs was also seen on the transcriptional level.
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this study shows that EMSY is increased and activates TSLP & CCL5 expression in eosinophilic esophagitis
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These CCL5 derivatives may now be tested against several inflammation-related pathologies where the CCL5:CCR5 axis plays a relevant role.
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The CCL5 In1.1T/C polymorphism may modulate pulmonary early-onset tuberculosis risk.
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We use CPRC prostate cancer model and demonstrate that endothelial cells secrete large amount of CCL5 and induces autophagy by suppressing AR expression in prostate cancer cell lines. Consequently, elevated autophagy accelerates focal adhesions proteins disassembly and promoted prostate cancer invasion. Inhibition of both CCL5/CCR5 signaling and autophagy significantly reduces metastasis in vivo
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CCL5, from endothelial cells, acts in a paracrine fashion on triple-negative breast cancer (TNBC) cells to enhance their migration, invasion, and metastasis. CCL5, in turn, accelerates TNBC cell secretion of PAI-1 and promotes TNBC cell metastasis, thus forming a positive feedback loop. Moreover, this enhanced metastatic ability is reversible and dependent on CCL5 signaling via the chemokine receptor, CCR5.
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high concentration of plasma CCL5 may promote EMT of breast cancer cells. Plasma CCL5 could be a promised candidate to predict chemotherapy response in NCT of LABC.
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The polymorphism of CCR1 rs3733096 and CCL5 rs3817656 are associated with spontaneous clearance of hepatitis C virus in Chinese Han population.
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Our results suggested that the CCL5 level was influenced collectively not only by the genotypes of -403G>A SNP and bacillary load but also by the treatment. Thus, CCL5 may be considered for the development of a diagnostic marker and also as an indicator of recovery.
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serum levels in active vitiligo significantly elevated compared to those in stable vitiligo patients
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these findings collectively indicate that TGF-beta regulates CCL5 expression in a stage-dependent manner during breast cancer progression
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KLF5-regulating cancer-associated fibroblasts affect gastric cancer cells progression by CCL5 secretion and activation of CCR5.
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Data show that plasminogen activator inhibitor-1 (PAI-1) and chemokine CCL5 (CCL5) overexpression promoted cell proliferation and migration in breast cancer cells.
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Among infants with lower CCL5 levels, the Haemophilus-dominant microbiota profile was associated with a higher risk of intensive care use and hospital length-of-stay >/=3 days compared to the Moraxella-dominant profile. Conversely, among those with higher CCL5 levels, there were no significant associations between the microbiota profiles and these severity outcomes
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The current study suggests that TLR3 signaling induces CCL5 expression via NF-kappaB and IRF3 in bile duct cells, and this pathway may be involved in the pathogenesis of BA.
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Study demonstrates that increased CCL5 expression was restricted to human mesenchymal glioblastoma (GBM) and suggests that CCL5 functions in an autocrine growth-promoting circuit, and establish a new receptor responsible for CCL5 function in mesenchymal glioblastoma cells.
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Study showed that bone stromal cells promoted prostate cancer progression through the secretion of CCL5. In vitro co-culture of bone stromal cells with prostate cancer cells induced the expression of CCL5, which promoted prostate cancer cell migration. CCL5 was found to have a key role in the progression of prostate cancer in the bone metastasis microenvironment.
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identifies the essential role of the chemoattractive cytokine CCL5 for liver disease progression and especially hepatocellular carcinoma development
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Breast cancer cell CCL5 mediates bone marrow independent angiogenesis via paracrine signaling.
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the present study has demonstrated a novel pathway involving CCl5/CCR1/beta-catenin/Slug, via which human Mesenchymal stem cells promotes colorectal cancer development.
