Background
To investigate the relation between interleukin-10 (IL-10) gene rs1800871 (A/G) polymorphism and spinal tuberculosis.
Material/Methods
A total of 129 patients with spinal tuberculosis (spinal tuberculosis group) and 106 healthy subjects receiving physical examination (control group) were enrolled in this study. The general data of these subjects were collected, and the C-reactive protein, erythrocyte sedimentation rate (ESR) and baseline hematologic function were examined. The rs1800871 (A/G) polymorphism in IL-10 gene was detected by TaqMan-MGB probe method.
Results
The C-reactive protein, ESR, white blood cell count, absolute neutrophil count and relative neutrophil count in spinal tuberculosis group were higher than those in control group, while the absolute lymphocyte count and relative lymphocyte count were lower than those in control group (
p
<0.05). Compared with AA genotype, GG and AG+GG genotypes showed statistically significant difference in distribution frequency (
p
<0.05), but no significant difference was detected between AG genotype and AA genotype (
p
>0.05). In spinal tuberculosis group, the frequency of G allele was higher than that of A allele (
p
<0.01). The C-reactive protein, ESR, white blood cell count and relative neutrophil count in GG genotype were increased compared with those in AG+GG genotype (
p
<0.05).
Conclusions
The rs1800871 (A/G) polymorphism in IL-10 gene is related to the susceptibility to spinal tuberculosis. Moreover, carrying G allele increases the risk of spinal tuberculosis.
Purpose: has been reported to be deregulated in many types of human cancers and play important roles in cancer genesis and progression. However, the biological roles of miR-761 in osteosarcoma (OS) and the underlying mechanisms remain largely unknown. Methods: The expression of miR-761 in OS tissues and cell lines was analyzed using RT-qPCR. A series of gain-of-function tests were performed, and status of malignancy was evaluated on basis of proliferation, migration, invasion, and apoptosis using different assays to determine the regulatory roles of miR-761 in OS cells in vivo and in vitro. Notably, the mechanisms underlying the action of miR-761 in the pathogenesis of OS were investigated using bioinformatic analysis, luciferase reporter assay, RT-qPCR and Western blotting. Results: The results showed that miR-761 expression was decreased in OS tissues and cell lines and is closely correlated with clinical stage and distant metastasis in OS patients. Patients with OS having low miR-761 expression showed worse prognosis compared to OS patients with high miR-761 expression. Restoring the miR-761 expression level decreased OS cell proliferation, migration, and invasion in vitro; promoted cell apoptosis in vitro; and impaired tumor growth in vivo. In addition, fibroblast growth factor receptor 1 (FGFR1) was found as a direct target gene of miR-761 in OS cells. Furthermore, silencing FGFR1 expression stimulated the tumor-suppressing roles of miR-761 upregulation in OS cells, whereas the activity of miR-761 overexpression in OS cells was abolished by the restoration of FGFR1 expression. Moreover, restoration of miR-761 expression deactivated the PI3K/ Akt pathway in vitro and in vivo. Conclusion: These results suggest that miR-761 plays anti-cancer roles in OS by directly targeting FGFR1 and deactivating the PI3K/Akt pathway. The newly identified miR-761/ FGFR1/PI3K/Akt pathway partially illustrates the mechanism of OS pathogenesis and presents a novel candidate therapeutic target for antitumor therapy.
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