BackgroundMicroRNA-223 (miR-223) has been shown to be a potential diagnostic and prognostic marker for several cancers. In addition, miR-223 has been reported to suppress osteosarcoma cell proliferation in vitro. However, the clinical value of miR-223 is still unknown.MethodsWe detected the expression of miR-223 expression in the serum of osteosarcoma patients and in osteosarcoma cancer cells using RT-PCR. We compared the serum expression of miR-223 with the clinicopathological characteristics and survival of osteosarcoma patients. Finally, we explored the role of miR-223 on the invasion of osteosarcoma cancer cells using cell migration and invasion assays.ResultsWe observed that the expression of miR-223 was significantly decreased in the serum of osteosarcoma patients and osteosarcoma cancer cells compared to healthy controls (P<0.01). Moreover, a receiver operating characteristic (ROC) curve analysis indicated that serum miR-223 is a potential diagnostic marker of osteosarcoma with an area under the ROC curve (AUC) of 0.956. Importantly, the patients with a lower expression of miR-223 tended to have distant metastasis (P<0.001) and a more advanced clinical stage (P<0.001). In addition, the survival time of patients with low miR-223 expression was significantly shorter compared to patients with high miR-223 expression (P<0.001). Furthermore, we found that miR-223 could inhibit the migration and invasion of osteosarcoma cells.ConclusionsmiR-223 might be related to the metastasis of osteosarcoma and could be used as a potential diagnostic and prognostic biomarker in osteosarcoma.

Rheumatoid arthritis (RA) is characterized by chronic inflammatory process that targets the synovial lining of diarthrodial joints. Programmed death 1 (PD-1) plays a key role in the negative regulation of the immune response. In the current study, we investigated the expression of PD-1 on peripheral CD4+ and CD8+ T cells in RA patients. Percentage of PD-1+ cells was measured by flow cytometry in 82 RA cases and 90 healthy controls. Results showed that PD-1 expression was significantly decreased in both peripheral CD4+ and CD8+ T cells in RA (p = 0.002 and p < 0.001, respectively). Similarly, serum levels of soluble PD-1 were also downregulated in RA cases. When comparing PD-1 level in RA patients with different clinical parameters, patients with positive C-reactive protein (CRP) revealed lower proportion of PD-1 on CD4+ and CD8+ T cells than those with negative CRP. Also, disease activity score of RA patients was inversely correlated with PD-1 expression on peripheral CD4+ and CD8+ T cells. These data suggested that PD-1 may act as a negative regulator in the pathogenesis and progression of RA.

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