In the recent years, matrix metalloproteinase 9 (MMP-9) has been focused on as an indicator of glioma grade and prognosis, especially in China. However, all results resulted in many conflicts. So, it is necessary to conduct a meta-analysis to secure a convincing correlation between MMP-9 and grade and prognosis. Eligible studies were included via multiple searches, and then odds ratios (ORs) and hazard ratios (HRs) with 95% confidence intervals (95% CIs) were estimated. Funnel plots were available for evaluation of publication bias. In addition, heterogeneity and sensitivity were also analyzed. In the present meta-analysis, 23 articles were allowed for inclusion with total 1,635 patients. Coincidentally, all studies were conducted in Chinese populations. High MMP-9 expression in gliomas was closely associated with high WHO grade (III+IV) (n = 22, OR = 5.25, 95% CI = 4.09-6.73; p = 0.000), while MMP-9 expression did not correlate to age (n = 4, OR = 1.02, 95 % CI = 0.67-1.54; p = 0.929) and gender (n = 5, OR = 0.91, 95% CI = 0.63-1.33; p = 0.632). Besides, overall survival analysis from two articles revealed MMP-9 expression significantly predicted 5-year-OS (HR = 6.44, 95% CI = 3.88-10.70; p = 0.000) in glioma patients. No heterogeneity and publication bias were observed across all studies. To conclude, this meta-analysis suggests MMP-9 is potently associated with high grade and poor 5 years prognosis, and MMP-9 test of glioma tissues should be established in department of pathology as a routine in clinical practice.

This study confirmed a considerably high prevalence of NDRD in type 2 diabetic patients with renal injury. As some cases of NDRD are readily treatable or remittable, we should consider renal biopsy in selected diabetic patients with renal involvement, especially in those with effective blood glucose control and the absence of diabetic retinopathy.

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The chemokine receptor CXCR4 and its ligand stromal cell-derived factor 1 (SDF-1) plays an important role in tumor progression and are associated with angiogenesis. Meanwhile, the implications of C23 in multiple signaling pathways have been also investigated. However, the effects of C23 on CXCR4 pathway in glioblastoma are not fully characterized. In the present study, C23 and CXCR4 of U87 cell line were inhibited by anti-C23 and anti-CXCR4 antibodies, respectively; and then C23 and CXCR4 siRNAs were used to knock down endogenous C23 and CXCR4, respectively. In addition, MTT assay was also introduced. Our data showed that either anti-C23 or anti-CXCR4 antibodies efficaciously repressed the phosphorylation levels of ERK (p < 0.000) and AKT (p < 0.000) compared with SDF-1 alone and control. As expected, either C23 or CXCR4 siRNAs indeed resulted in C23 and CXCR4 knockdown and further suppressed the expression of p-ERK and p-AKT. Most importantly, immunoprecipitation revealed C23 interacted with CXCR4 once U87 was exposed to SDF-1 treatment. In addition, MTT assay identified that C23 or CXCR4 siRNAs could obviously decreased cell proliferation capacity (p = 0.002). In conclusion, our results suggest that C23 plays a crucial role in activation of SDF-1-induced ERK and PI3K/AKT pathways via interacting with CXCR4. Furthermore, C23 could be recommended as an important element in glioblastoma development and a new target for glioblastoma treatment.

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