Association between glutathione S-transferase T1 null genotype and glioma susceptibility: a meta-analysis.

The relationship between genetic polymorphisms of glutathione S-transferase (GST) and the development of glioma has been investigated in several epidemiologic studies. However, these studies report inconsistent results. In order to get this precise result, a meta-analysis was conducted by calculating the pooled odds ratios (OR) and the 95% confidence intervals (95 % CI). Eleven case-control research studies with a total of 2,416 glioma cases and 4,850 controls were included into this meta-analysis. The combined results based on all studies showed that there was no significant association between the GSTT1 null allele and glioma risk (OR = 1.188, 95% CI = 0.929­1.520, P(heterogeneity) = 0.003, P = 0.170). In the subgroup analysis, the same results were found in our work. There was no risk of publication bias in this meta-analysis. Our results suggest that GSTT1 null genotype was not associated with the increased risk of glioma.

Effects of tetrandrine on glioma cell malignant phenotype via inhibition of ADAM17.

Tetrandrine (TET), a bisbenzylisoquinoline alkaloid isolated from the root of Hang-Fang-Chi (Stephania tetrandra S. Moore), exhibits broad pharmacological effects, including antitumor activity in various malignant neoplasms. Recently, the beneficial effects of TET on cytotoxicity towards tumor cells, radiosensitization, circumventing multidrug resistance, normal tissue radioprotection, and antiangiogenesis have been examined extensively. However, the potential molecular mechanisms of the effect on glioma of TET are yet unknown. This study is explored to evaluate whether TET can inhibit cell proliferation, invasion, and the possible underlying mechanisms in glioma U87 cell. In the present study, cell proliferation was determined by using the Cell Counting Kit-8 (CCK-8) viability assay. The invasion and migration were evaluated by means of wound-scratch assay and Matrigel-Transwell methods. The mRNA expression and protein expression of ADAM metallopeptidase domain 17 (ADAM17) in glioma cell lines and glioma samples were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting, respectively. Moreover, the expression of epidermal growth factor receptor (EGFR)/p-EGFR and AKT/p-AKT was studied to clarify the molecular mechanism. Our results suggested that TET inhibited cell proliferation in a dose- and time-dependent manner, and cell migration and invasion in vitro. In addition, our results indicated that ADAM17 expression significantly increased in glioma compared to nontumored human brain tissue and according to the histopathological grade of glioma. Western blot analysis showed that protein expressions of ADAM17, p-EGFR, and p-AKT were inhibited by TET in U87 cells. These data also suggest that suppression of ADAM17 and downregulation of EGFR-phosphoinositide-3-kinase (PI3K)-AKT signaling pathways may contribute to TET-induced decrease of proliferation, migration, and invasiveness.