A meta-analysis of carotid endarterectomy versus stenting in the treatment of symptomatic carotid stenosis.

BACKGROUND: Carotid stenosis is one of the common reasons for patients with ischemic stroke, and the two invasive options carotid endarterectomy (CEA) and carotid artery stenting (CAS) are the most popular treatments. But the relative efficacy and safety of the methods are not clear. METHODS: About 521 articles related to CAS and CEA for carotid stenosis published in 1995 - 2011 were retrieved from MEDLINE, Cochrane Library (CL), and China National Knowledge Infrastructure (CNKI) China Journal Full-Test database. Of them, eight articles were chosen. Meta-analysis was used to assess the relative risks. RESULTS: The eight studies included 3873 patients with symptomatic carotid artery stenosis, including 1941 cases in the carotid stent angioplasty group, and 1932 cases in the carotid endarterectomy group. Fixed effect model analysis showed that within 30 days of incidence of all types of strokes, surgery was significantly highly preferred in CAS patients (CAS group) than the CEA patients (CEA group), and the difference was statistically significant (relative ratio (RR) = 1.80, 95% confidence interval (CI): 1.380 - 2.401, P < 0.0001). But the incidence of death in the two groups is not showed and is not statistically significant after 30 days (RR = 1.52, 95%CI: 0.82 - 2.82, P = 0.18). The rate of cranial nerve injury in the CAS group is lower than the CEA group (RR = 0.14, 95%CI: 0.05 - 0.43, P = 0.0005). The incidence of CAS patients with myocardial infarction is lower than the CEA group after 30 days, but statistically meaningless (RR = 0.22, 95%CI: 0.05 - 1.02, P = 0.05). The stroke or death in CAS patients were higher than the CEA group after 1 year of treatment (RR = 2.58, 95%CI: 1.03 - 6.48, P = 0.04). CONCLUSIONS: Compared to CAS, carotid endarterectomy is still the preferred treatment methodology of symptomatic carotid artery stenosis. Future meta-analyses should then be performed in long-term follow-up to support this treatment recommendation.

MiR-21 modulates hTERT through a STAT3-dependent manner on glioblastoma cell growth.

BACKGROUND AND PURPOSE: As an important oncogenic miRNA, miR-21 has been reported to play crucial roles in glioblastoma (GBM) carcinogenesis. However, the precise biological function and molecular mechanism of miR-21 in GBM remain elusive. This study is designed to explore the mechanism of miR-21 involved in the control of GBM cell growth. METHODS AND RESULTS: MTT assay, cell cycle analysis, and apoptosis analysis showed that reduction of miR-21 inhibited cell growth in U87 and LN229 GBM cells. Further, reduction of miR-21 decreased the expression of human telomerase reverse transcriptase (hTERT) and repressed STAT3 expression and STAT3 phosphorylation. STAT3 inhibition led to a remarkable depletion of hTERT at both mRNA and protein levels by binding to the hTERT gene promoter by performing luciferase reporter assay and chromatin Immunoprecipitation PCR. Finally, knockdown of miR-21 considerably inhibited tumor growth and diminished the expression of STAT3 and hTERT in xenograft model. CONCLUSION: Our findings indicate that miR-21 regulates hTERT expression mediated by STAT3, therefore controlling GBM cell growth.

MicroRNA-21 expression is regulated by ß-catenin/STAT3 pathway and promotes glioma cell invasion by direct targeting RECK.

AIMS: MicroRNA-21 (miR-21) expression is increased in many types of human malignancy, including glioma. Recent studies report that miR-21 regulates cell invasion by targeting RECK, however, the underlying transcriptional regulation of miR-21 in glioma cells remains elusive. RESULTS: Here, we identify a positive correlation between miR-21 expression and pathological grade in glioma tissues. We demonstrate that ß-catenin pathway regulates miR-21 expression in human umbilical vein endothelial cell and glioma cells, and that this regulation is signal transducer and activator of transcription 3 (STAT3)-dependent. Further, chromatin immunoprecipitation and luciferase reporter analysis demonstrate that miR-21 is controlled by an upstream promoter containing a conserved STAT3 binding site. Notably, knockdown of miR-21-inhibited cell invasion by increasing RECK expression and decreased tumor growth in a xenograft model. CONCLUSION: These data provide compelling evidence that ß-catenin regulation of miR-21 via STAT3 plays a role in glioma cell invasion and proliferation and indicate that STAT3 is a potential therapeutic target for glioma intervention.