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miR-128 interacts with CCL18 3'UTR, reducing its expression in malignant melanoma.
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AMAP1 mediated CCL18-induce activation of NF-kappaB and promoted breast cancer metastasis.
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results of the study indicate that there could be a relationship between the expression of CCL-18 in nasal turbinate mucosa and the severity of allergic rhinitis
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chemokine CCL18 can be a mediator of peritoneal membrane failure associated with peritonitis episodes as well as providing a new potential therapeutic target.
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CCL18 was up-regulated in diffuse large B cell lymphoma and related to poor prognosis
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Serum C-C motif chemokine ligand 18 (CCL18) was elevated in patients with epithelial ovarian cancer (EOC) and could serve as a new tumor biomarker, which also predicted a poor survival of the patient.
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In advanced lung adenocarcinoma, infiltration of CCL18(+) tumor-associated macrophages (TAMs) was increased and higher expression of CCL18 by TAMs was associated with a favorable prognosis in lymph-node positive NSCLC
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This study study discovered a positive feedback loop between CTGF and CCL18 in hepatocellular carcinoma metastasis.
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All patients with NPC1 mutations had high ChT activity, high CCL18/PARC concentrations and/or Niemann-Pick disease type C suspicion index scores >/=70.
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findings suggest that these pulmonary markers could be useful to assess CAP severity and, especially YKL-40 and CCL18 by helping predict CAP caused by atypical pathogens
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PARC activation of neutrophils by sterile immunogenic dying cells drives neutrophil-mediated residual cell killing.
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Matrigel invasion assays revealed that tumor ECM-educated macrophages efficiently stimulated cancer cell invasion through a mechanism involving CCL18.
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Our results indicate that CCL18 acts in an autocrine manner via Akt activation to stimulate oral squamous cell carcinoma cell growth and invasion during disease progression
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Our data indicate that hypoxic inhibition of JMJD3 activity reduces demethylation of H3K27me3, nucleosome removal, and hence induction of the STAT6 target gene CCL18, while induction of other STAT6-inducible genes such as SPINT2 remained unaffected by JMJD3.
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There was no association between serial CCL18 concentrations with tumor response and overall survival.
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CCL-18 is a promising biomarker in COPD, as it is associated with frequency of exacerbations, particularly with severe COPD exacerbations requiring hospitalization, as well as with functional parameters and symptom scores.
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Data suggested that CCL18 upregulated Slug expression to promote epithelial-mesenchymal transition (EMT) and stem cell-like features by activating the mTOR pathway in oral cancer.
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An increased lung protein expression of PARC in chronic obstructive pulmonary disease patients
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CCL18 can increase the invasive ability of non-small cell lung cancer cells by binding to its receptor Nir1.
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Results demonstrate that high levels of CCL18 are present in ovarian cancer (OC) ascites and that CCL18 is an important component of ascites for the ascites-mediated migration of OC cells. Ascites and CCL18 stimulate the phosphorylation and expression of Pyk2, which is critical for mediated CCL18-induced migration.
