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ABSTRACT: BACKGROUND: Meningioma is the second most common primary tumor of the central nervous system, and multiple genetic and environmental factors contribute to its etiology. Methylene tetrahydrofolate reductase (MTHFR) is a pivotal enzyme in folate metabolism. We conducted a case-control study to investigate the association of the MTHFR gene and meningioma in a Han population in northern China. METHODS: We genotyped two SNPs (C677T and A1298C) using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). In this study 317 meningioma patients were compared to 320 normal controls. Data were analyzed by SPSS 13.0 and HaploView software. RESULTS: We found a significant difference in the frequency distribution of 677CC and 677TT between cases and control groups; another SNP exhibited no differences in any genotype between the two cohorts. CONCLUSION: The results revealed that variations of the MTHFR gene were associated with meningioma; this finding indicates that the MTHFR gene potentially plays an important role in the pathogenesis of meningioma in the Northern Chinese Han population.
Gene 12/2012; · 2.34 Impact Factor
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Lingchao Chen,
Junhe Zhang, Yan Feng,
Ruiyan Li,
Xu Sun,
Wenzhong Du,
Xinyin Piao,
Hanbing Wang,
Dongbo Yang,
Ying Sun,
Xianfeng Li,
Tao Jiang,
Chunsheng Kang,
Yongli Li,
Chuanlu Jiang
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ABSTRACT: MET, the receptor for hepatocyte growth factor receptor (HGF), has been reported to trigger multiple and sometimes opposing cellular responses in various types of tumor cells. It has been implicated in the regulation of tumor-cell survival, proliferation, angiogenesis, invasion and metastasis. However, the MET regulatory mechanism in glioma is not well known. MicroRNAs are a class of small noncoding RNAs that play important roles in a variety of biological processes including human cancers. In this study, we used computational and expressional analysis to identify that the 'seed sequence' of miR-410 matched the 3' UTR of the MET mRNA. Besides, the expression of miR-410 was inversely associated with MET in human glioma tissues. Using luciferase and western blot assay, we certified that miR-410 directly targeted MET in glioma cells. While restoring expression of miR-410 led to proliferation inhibition and reduced invasive capability in glioma cells. Furthermore, we showed that miR-410 played an important role in regulating MET-induced AKT signal transduction. While downregulation of MET by RNAi, we observed that MET knockdown resulted in effects similar to that with miR-410 transfection in glioma cells. Our findings suggest that miR-410, a direct regulator of MET, may function as a tumor suppressor in human gliomas.
The international journal of biochemistry & cell biology 06/2012; 44(11):1711-7. · 4.89 Impact Factor
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Lingchao Chen,
Xiaofeng Wang,
Hanbing Wang,
Yongli Li,
Wei Yan,
Lei Han,
Kailiang Zhang,
Junxia Zhang,
Yongzhi Wang, Yan Feng,
Peiyu Pu,
Tao Jiang,
Chunsheng Kang,
Chuanlu Jiang
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ABSTRACT: MicroRNAs are strongly implicated in cancer but their specific roles and functions in the major cancers have yet to be fully elucidated. In this study, we defined the expression and function of miR-137, which we found to be downregulated in glioma samples and glioma cells by qRT-PCR. Ectopic expression of miR-137 in glioma cell lines inhibited proliferation and invasion. Using computational and expression analysis, Cox-2 was identified as a candidate target of miR-137. Reporter assay with 3'UTR of Cox-2 cloned downstream of the luciferase gene showed reduced luciferase activity in the presence of miR-137, providing strong evidence that miR-137 was a direct regulator of Cox-2. Expression analysis further revealed that Cox-2 was elevated in glioma and associated with survival of patients. Furthermore, we observed that Cox-2 knockdown resulted in effects similar to those with miR-137 transfection in glioma cells. In conclusion, our study demonstrates that miR-137 deregulation is common in glioma, and restoration of its function inhibits cell proliferation and invasion, suggesting that miR-137 may act as a tumour suppressor.
European journal of cancer (Oxford, England: 1990) 03/2012; 48(16):3104-11. · 4.12 Impact Factor
