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CXCL5-overexpressing tumors had reduced lung metastasis compared with control tumors. Neutrophil depletion reversed this effect. In vitro, unstimulated lung-derived neutrophils had higher levels of reactive oxygen species compared with tumor-associated neutrophils, and CXCL5 stimulation further increased reactive oxygen species levels
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Decreased wound exudate ENA-78 was independently associated with wound healing of patients with diabetic foot. Exudate ENA-78 level is implicated as a novel predictor of wound healing in patients with diabetic foot ulcers.
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CXCL5-overexpressing tumors recruited high amounts of neutrophils and exhibited significantly increased lymphangiogenesis in xenograft SCID mouse model. Clinically, CXCL5-overexpressing melanomas had significantly increased lymph node metastases. In human patient samples CXCL5 expression positively correlated with numbers of neutrophils in stage T4 primary melanoma, and the occurrence of locoregional metastasis.
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CXCL5 may contribute to a dominant role in uterine cervix cancer progression; at the gene level, CXCL5 overexpression regulated the expression of tumor-related genes
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Sensitivity and specificity of serum CXCL5 were found to be low as a result of the ROC analysis.
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Serum CXCL5 levels from pemphigus vulgaris patients are significantly higher than those in bullous pemphigoid patients and healthy controls.
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These data demonstrated that CXCL5 expression was upregulated in prostate cancer tissues and that exogenous CXCL5 protein exposure or CXCL5 overexpression promoted malignant phenotypes of prostate cancer cells in vitro and in vivo.
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activated CXCL5-CXCR2 axis contributes to the metastatic phenotype of PTC cells by modulating Akt/GSK-3beta/beta-catenin pathway
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study elucidates the important role of CXCL5 in the progression and prognosis of NSCLC. These findings suggested that CXCL5 might be a potential biomarker and novel therapeutic target for lung cancer
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PERK-p-eIF2alpha pathway could suppress metastasis in triple-negative breast cancer by inhibiting expression of PDL1 and CXCL5 in tumor cells.
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Mechanistically, AR modulated cytokine CXCL5 expression by altering AKT --> NF-kappaB signaling, and interruption of AKT --> NF-kappaB --> CXCL5 signaling using either specific inhibitors or siRNA suppressed AR-enhanced EC recruitment and AR-EC-promoted RCC progression.
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Curcumin suppressed CXCL5 expression by direct inhibition of IKKbeta phosphorylation, and inhibition of p38 MAPK via induction of negative regulator MKP-1.
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The CXCL5 and the overexpression of miR-141 reduced levels of MMP-2 and MMP-9 in tumor necrosis factor-alpha-treated HT29 cells by means of repressing the inhibitory AKT.
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CXCL5 may promote mitomycin resistance by activating EMT and NF-kappaB pathway. Thus, this study identifies CXCL5 as a novel chemoresistance-related marker in non-muscle invasive bladder cancer
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findings for the first time provided evidence that ENA78 may play a key role of mediator in pathogenesis of Major Depressive Disorder(MDD) and in the mechanism of vinlafaxine effects on MDD.
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Two haplotype blocks, one upstream to the coding region of UGT2A1 (rs146712414, P = 9.1 x 10(-5); odds ratio [OR], 1.34; 95% confidence interval [CI], 1.16-1.56) and one downstream of the genes PF4/PPBP/CXCL5 (rs1595009, P = 1.3 x 10(-4); OR, 1.32; 95% CI, 1.15-1.52), were associated with AgP.
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our findings support CXCL5 as a promoter of colorectal cancer metastasis and a predictor of poor clinical outcomes in colorectal cancer patients.
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CXCL5 levels were decreased in LSCC patient serum.
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a finely tuned balance between the GAG-bound dimer and free soluble monomer regulates CXCL5-mediated receptor signaling and function.
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CXCL5 plays a promoting role in glioma in autocrine- and paracrine-dependent manners.