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The role of protein arginine-methyltransferase 1 in gliomagenesis
( Shan Wang ),( Xiao Chao Tan ),( Bin Yang ),( Bin Yin ),( Jian Gang Yuan ),( Bo Qin Qiang ),( Xiao Zhong Peng ) 생화학분자생물학회(구 한국생화학분자생물학회) 2012 BMB Reports Vol.45 No.8
Protein arginine methyltransferase 1 (PRMT1), a type-I arginine methyltransferase, has been implicated in diverse cellular events. We have focused on the role of PRMT1 in gliomagenesis. In this study, we showed that PRMT1 expression was up-regulated in glioma tissues and cell lines compared with normal brain tissues. The knock-down of PRMT1 resulted in an arrest in the G1-S phase of the cell cycle, proliferation inhibition and apoptosis induction in four glioma cell lines (T98G, U87MG, U251, and A172). Moreover, an in vivo study confirmed that the tumor growth in nude mouse xenografts was significantly decreased in the RNAi-PRMT1 group. Additionally, we found that the level of the asymmetric dimethylated modification of H4R3, a substrate of PRMT1, was higher in glioma cells than in normal brain tissues and decreased after PRMT1 knock-down. Our data suggest a potential role for PRMT1 as a novel biomarker of and therapeutic target in gliomas. [BMB Reports 2012; 45(8): 470-475]
MicroRNA-214-mediated UBC9 expression in glioma
( Zhi Qiang Zhao ),( Xiao Chao Tan ),( Ani Zhao ),( Li Yuan Zhu ),( Bin Yin ),( Jiang Ang Yuan ),( Bo Qin Qiang ),( Xiao Zhong Peng ) 생화학분자생물학회(구 한국생화학분자생물학회) 2012 BMB Reports Vol.45 No.11
It has been reported that ubiquitin-conjugating enzyme 9 (Ubc9), the unique enzyme2 in the sumoylation pathway, is up-regulated in many cancers. However, the expression and regulation of UBC9 in glioma remains unknown. In this study, we found that Ubc9 was up-regulated in glioma tissues and cell lines compared to a normal control. UBC9 knockdown by small interfering RNA (siRNA) affected cell proliferation and apoptosis in T98G cells. Further experiments revealed that microRNA (miR)-214 directly targeted the 3` untranslated region (UTR) of UBC9 and that there was an inverse relationship between the expression levels of miR-214 and UBC9 protein in glioma tissues and cells. MiR-214 overexpression suppressed the endogenous UBC9 protein and affected T98G cell proliferation. These findings suggest that miR-214 reduction facilitates UBC9 expression and is involved in the regulation of glioma cell proliferation.