It has been reported that glioma has a higher morbidity and mortality than other types of malignant brain tumor. While glioma has been extensively researched, the exact molecular mechanisms of its genesis and progression have remained to be fully elucidated. In order to explore a novel glioma-associated pathway which may represent a therapeutic target, 61 pairs of tumor tissues and adjacent normal tissues of glioma patients were collected and subjected to reverse-transcription quantitative polymerase chain reaction analysis, indicating that the relative expression of microRNA (miR)-128-3p was significantly decreased in the tumor tissues. However, the expression of neuronal pentraxin 1 (NPTX1) was obviously elevated. Through a bioinformatics analysis using Targetscan and transfection experiments, it was confirmed that NPTX1 was targeted by miR-128-3p. In the U251 human glioma cell line, transfection with miR-128-3p mimics increased the levels of phosphorylated insulin receptor substrate 1 (p-IRS-1), phosphoinositide-3 kinase (PI3K) and p-AKT, as demonstrated by western blot analysis. In addition, the proliferation rate of the cells was notably decreased following transfection with miR-128-3p mimics. Conversely, transfection with miR-128-3p inhibitor significantly increased the levels of p-IRS-1, PI3K and p-AKT, accompanied by an elevated proliferation rate of the cells. Therefore, it was indicated that miR-128-3p could reversely regulate NPTX1 expression. After the expression of NPTX1 was inhibited with specific small interfering RNA, the levels of p-IRS-1, PI3K and p-AKT were obviously decreased, while the expression of miR-128-3p was not significantly changed. Overall, it was concluded that miR-128-3p suppresses glioma through the NPTX1/IRS-1/PI3K/AKT signaling pathway.

Background. To comprehensively assess the efficacy and safety of whole-brain radiotherapy (WBRT) combined with gefitinib/erlotinib for treatment of brain metastases (BM) from non-small-cell lung cancer (NSCLC). Methods. Databases including PubMed, EMBASE.com, Web of Science, and Cochrane Library were searched from inception to April 12, 2015. Studies on randomized controlled trials (RCTs) and case-control trials comparing WBRT combined with gefitinib/erlotinib versus WBRT alone for BM from NSCLC were included. Literature selection, data extraction, and quality assessment were performed independently by two trained reviewers. RevMan 5.3 software was used to analyze data. Results. A total of 7 trials involving 622 patients were included. Compared with WBRT alone or WBRT plus chemotherapy, WBRT plus gefitinib/erlotinib could significantly improve response rate (OR = 2.16, 95% CI: 1.35–3.47; P = 0.001), remission rate of central nervous system (OR = 6.06, 95% CI: 2.57–14.29; P < 0.0001), disease control rate (OR = 3.34, 95% CI: 1.84–6.07; P < 0.0001), overall survival (HR = 0.72, 95% CI: 0.58–0.89; P = 0.002), and 1-year survival rate (OR = 2.43, 95% CI: 1.51–3.91; P = 0.0002). In adverse events (III-IV), statistically significant differences were not found, except for rash (OR = 7.96, 95% CI: 2.02–31.34; P = 0.003) and myelosuppression (OR = 0.19, 95% CI: 0.07–0.51; P = 0.0010). Conclusions. WBRT plus gefitinib/erlotinib was superior to WBRT alone and well tolerated in patients with BM from NSCLC.

Demonstrated herein is a Pd-catalyzed ortho-CÀ H olefination of benzenesulfonamides using 7-azaindole as the directing group. This reaction proceeds with exclusive ortho selectivity, high efficiency and broad substrate scope. This method also provides access to sulfonic acids and ortho-alkylated sulfonamides. Control experiments provides some insightful evidences to the mechanism and the plausible catalytic cycle is proposed to go through a unique seven-membered palladacycle species.