Abstract. Matrix metalloproteinase-2 (MMP-2) is a member of the MMP family, which is associated with numerous types of cancer. Although it has been widely reported, the prognostic value of MMP-2 expression in prostate cancer (PCa) remains controversial. Thus, the present meta-analysis was conducted to investigate the association and prognostic value of MMP-2 expression in PCa. PubMed, Cochrane Library and the China National Knowledge Infrastructure databases were searched for all the published case-control studies on the association between MMP-2 expression and PCa until July 2015. The odd ratios (ORs) and 95% confidence intervals (CIs) were used to estimate the association of MMP-2 expression and PCa. ORs and 95% CIs were applied to clarify this association. Several subgroup analyses were also conducted according to different indexes in the case group. In total, 8 studies including 675 patients were included in the final meta-analysis. The results of the meta-analysis showed that MMP-2 expression in the PCa group was significantly higher than that in the benign prostatic hyperplasia (BPH) group (95% CI, 0.06-0.15; Z=10.48; P<0.00001). Furthermore, MMP-2 expression was significantly associated with Gleason Score (95% CI, 0.18-0.68; Z=3.09; P=0.002) and clinical stages (95% CI, 0.12-0.82; Z=2.36; P=0.02), and not significantly associated with Gleason score serum prostate specific antigen (95% CI, 0.30-1.66; Z=0.80; P=0.43). In conclusion, MMP-2 is overexpressed in PCa tissues compared with BPH. The expression of MMP-2 was significantly associated with the grade of PCa malignancy.

Roscovitine is a cyclin-dependent kinase inhibitor, which has been previously investigated for its anticancer effects. It has also been confirmed that roscovitine can downregulate the expression of myeloid cell leukemia-1 protein to inhibit inflammation. In the present study, roscovitine was used to treat inflammation in lipopolysaccharide (LPS)-induced model mice. At the cellular level, Leydig cells isolated from mouse testis were assessed for inflammatory factors. It was revealed that roscovitine successfully reduced inflammation-associated injury induced by LPS pretreatment. At the molecular level, roscovitine was found to exert this effect through promotion of adenosine monophosphate-activated protein kinase phosphorylation. To the best of our knowledge, the present study was the first to suggest that roscovitine has a protective role in Leydig cells through its anti-inflammatory action.

Background Dysregulation of cancer-associated fibroblasts (CAFs) still greatly challenges the treatments for bladder cancer (BC), where exosomal miRNAs derived from CAFs are one of the essential effectors for tumor progression. miR-93-5p is reported to be upregulated in BC, however, it is barely investigated in BC-derived CAFs. Method The CAF markers were immunofluorescent-labeled and examined by western blotting assay in CAFs and normal fibroblasts (NFs). CAFs- and NFs-derived exosomes (CAFs-exo/NFs-exo) were authenticated by transmission electron microscope and nanoparticle tracking analysis. Cell viability was determined by cell counting kit-8 assay, and cell mobility was evaluated by wound healing and transwell assays. Real-time quantitative PCR was used to quantify the RNA expressions, and a western blotting assay was used for protein expression. Interaction between miR-93-5p and Platelet-Activating Factor Acetylhydrolase IB Subunit Beta (PAFAH1B1) was verified by luciferase reporter assay. HE staining assay was applied to assess the histological changes of xenografts. Results CAFs-exo notably enhanced cell mobility and the expression levels of miR-93-5p of BC cells compared to NFs-exo. However, inhibition of miR-93-5p in CAFs-exo exhibited attenuated pro-metastatic ability on BC cells. PAFAH1B1 was one of the predicted targets of miR-93-5p, whose mRNA level was most significantly downregulated after miR-93-5p transfection. The interaction between PAFAH1B1 and miR-93-5p was verified, and miR-93-5p negatively regulated the protein level of PAFAH1B1. Overexpression of PAFAH1B1 could efficiently reverse the effects of miR-93-5p mimic on BC cell mobility. Finally, inhibition of miR-93-5p was proved to impair the carcinogenic function of CAFs-exo in vivo. Conclusion Exosomal miR-93-5p derived from CAFs confers oncogenicity on BC cells via sponging PAFAH1B1, suggesting a novel therapeutic strategy for BC.