Chemokines are a family of small 8-10 kDa inducible cytokines. Initially characterized as chemotactic factors, they are now considered to affect not just cellular recruitment. CX3CL1 is a unique chemokine that can exist in a soluble form, as a chemotactic cytokine, or in a membrane-attached form that acts as a binding molecule. Recently, the effects of CX3CL1 on diseases, such as inflammation and cancer, have been supported and confirmed by numerous publications. However, due to its dual effects, CX3CL1 exerts numerous effects on pathophysiological conditions that have both negative and positive consequences on pathogenesis and outcome. This review article summarizes the important scientific and clinical data that now point to a critical role for CX3CL1 in diseases.

BackgroundThe cervical sagittal parameters of the normal population and the impact of disc degeneration on cervical sagittal alignment have not been clearly defined yet. This study is applied to investigate the characteristics and relationships of cervical sagittal parameters in normal adults and patients with cervical disc degeneration.MethodsWe reviewed 50 normal control subjects (normal group, NG) and 50 patients with cervical disc degeneration (degeneration group, DG), who had both cervical MRI and radiographs obtained together, between January 2010 and September 2015. Data including C2–7 lordosis (CL), T1 slope (T1S), thoracic inlet angle (TIA), neck tilt (NT), C2–7 sagittal vertical axis (C2–7 SVA), cervical tilting, and cranial tilting on cervical radiographs were collected and analyzed.ResultsT1S in the NG was significantly greater than in the DG (P < 0.05), while NT and C2–7 SVA in the NG were significantly lower than in the DG (P < 0.01 and P < 0.05, respectively). T1S positively correlated with CL in both groups (Pearson correlation coefficients of 0.588 in the NG and 0.504 in the DG). No significant difference was seen in TIA between the NG and DG.ConclusionsT1S was involved in the occurrence and development of cervical disc degeneration, and TIA could be considered as a constant morphological parameter in both the normal population and cervical disc degeneration patients.Electronic supplementary materialThe online version of this article (10.1186/s12891-018-1951-8) contains supplementary material, which is available to authorized users.

The present study investigated the role of C-X3-C motif chemokine ligand 1 (CX3CL1) in lung cancer cell migration and invasion and its potential mechanism. The expression levels of C-X3-C motif chemokine receptor 1 (CX3CR1) in six human lung cancer cell lines and one human bronchial epithelial cell line were assessed using reverse transcription-quantitative polymerase chain reaction and western blotting. Cell proliferation was assessed using the Cell Counting Kit-8 assay. Cell migration and invasion were examined using the Transwell assay, with and without Matrigel, respectively. The signaling pathway activated by CX3CL1 was analyzed via western blotting and inhibitory migration and invasion assays. CX3CR1 was expressed in the six lung cancer cell lines and one normal lung cell line. The lung cancer cell line, H460, was selected for further study. CX3CL1 did not significantly affect H460 proliferation; however, CX3CL1 did significantly enhance the migration and invasion of H460 cells. The Src/focal adhesion kinase (FAK) signaling pathway was activated in a time-dependent manner upon stimulation of CX3CL1. However, blocking Src activity with saracatinib prevented CX3CL1-mediated cell migration and invasion. Therefore, the findings indicated that CX3CL1 promotes lung cancer cell migration and invasion in vitro, and the Src/FAK signaling pathway serves a vital role in this process.

The activation of a delayed secondary cascade of unsatisfactory cellular and molecular responses after a primary mechanical insult to the spinal cord causes the progressive degeneration of this structure. Disturbance of ionic homeostasis is part of the secondary injury process and plays an integral role in the early stage of spinal cord injury (SCI). The secondary pathology of SCI is complex and involves disturbance of the homeostasis of K(+) , Na(+) , and Ca(2+) . The effect of ion channel blockers on chronic SCI has also been proved. In this Mini-Review, we provide a comprehensive summary of the effects of ion channel blockers on the natural responses after SCI. Combination therapy is based on the roles of ions and disturbance of their homeostasis in SCI. The effects of ion channel blockers suggest that they have potential in the treatment of SCI, although the complexity of their effects shows that further knowledge is needed before they can be applied clinically.

Key Points Question What is the immunogenomic landscape of osteosarcoma? Findings In this genetic association study based on 84 samples from The Cancer Genome Atlas, 14 immune-related genes associated with survival in osteosarcoma were identified. Meaning These findings suggest that a diagnostic risk score based on immune-related gene expression profiles may be useful to planning individualized therapies for osteosarcoma.

ObjectivesThe aim of our study was to investigate the general mechanism of spinal metastases from five different primary cancers: lung cancer, breast cancer, liver cancer, prostate cancer, and kidney cancer.ResultsFrom microarray analysis and validation by real-time polymerase chain reaction, CX3C chemokine ligand 1 (CX3CL1) appeared to be a potential chemokine widely involved in the process of spinal metastases. Further studies revealed that, compared with normal controls, serum samples from patients with spinal metastases from the lung (P < 0.01), kidney (P < 0.05) and prostate (P < 0.05) contained significantly higher levels of CX3CL1, whereas those from patients with spinal metastases from the liver and breast had a tendency to contain higher levels of CX3CL1 but without significance. Immunohistochemical staining for the expression of CX3C chemokine receptor 1 (CX3CR1), the receptor for CX3CL1, in all spinal metastases samples showed negative staining.Materials and MethodsCancellous bone in the spine from patients with and without spinal metastases was collected for mRNA microarray study, and then differentially expressed mRNAs related to chemokines were further confirmed by real-time polymerase chain reaction. Enzyme linked immunosorbent assay was used to detect the serum level of the selected chemokines and immunohistochemical staining was used to detect the expression level of corresponding receptors in tumor.ConclusionsOur present study showed that CX3CL1 is associated with the process of spinal metastases from different primary cancers.

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The present study aimed to examine the universal gene expression signature and the underlying molecular mechanisms involved in the progression of carotid atherosclerotic plaques. The gene expression dataset, GSE28829, containing 13 early and 16 advanced carotid atherosclerotic plaques was selected for analysis. The differentially expressed genes (DEGs) were identified and analyzed using bioinformatics analyses, including cluster analysis, Gene Ontology (GO) and pathway enrichment analyses. Finally, a protein-protein interaction (PPI) was constructed and analyzed. A total of 515 downregulated and 243 downregulated DEGs were identified. The cluster analysis revealed two separate two groups. In addition, the GO terms enriched by the upregulated DEGs were associated with immune response, and the downregulated DEGs were associated with cell adhesion. The upregulated DEGs were enriched in pathways associated with signaling in the immune system, and the downregulated DEGs were enriched in pathways associated with muscle contraction. In the PPI network analysis, ITGAM and ACTN2 had the highest decrees of connectivity in the upregulated and downregulated DEGs, respectively. These findings suggested that deregulation of the immune system and smooth muscle cell cytoskeleton accelerates the progression of carotid atherosclerotic plaques. The DEGs identified may offer potential in the prevention and treatment of atherosclerosis in the carotid artery.