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Implicated Role of Liposarcoma Related Fusion Oncoprotein TLS-CHOP in the Dysregulation of Arginine-Specific Methylation through PRMT1
Cell Biology
Volume 1, Issue 2, July 2013, Pages: 18-23
Received: Oct. 3, 2013; Published: Dec. 10, 2013
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Authors
Kenta Fujimoto, Division of Gene Structure and Function, Research Center for Genomic Medicine, Saitama Medical University, 1397-1 Yamane, Hidaka-shi, Saitama 350-1241, Japan
Shigeki Arai, Division of Gene Structure and Function, Research Center for Genomic Medicine, Saitama Medical University, 1397-1 Yamane, Hidaka-shi, Saitama 350-1241, Japan
Maki Matsubara, Division of Gene Structure and Function, Research Center for Genomic Medicine, Saitama Medical University, 1397-1 Yamane, Hidaka-shi, Saitama 350-1241, Japan
Kun Du, Division of Gene Structure and Function, Research Center for Genomic Medicine, Saitama Medical University, 1397-1 Yamane, Hidaka-shi, Saitama 350-1241, Japan
Yasuto Araki, Department of Rheumatology and Applied Immunology, Faculty of Medicine, Saitama Medical University, 38 Morohongo, Moroyama, Iruma-gun, Saitama 350-0495, Japan
Akio Matsushita, Division of Gene Structure and Function, Research Center for Genomic Medicine, Saitama Medical University, 1397-1 Yamane, Hidaka-shi, Saitama 350-1241, Japan; Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, 1-20-1 Handayama, Hamamatsu, Shizuoka 431-3192, Japan
Riki Kurokawa, Division of Gene Structure and Function, Research Center for Genomic Medicine, Saitama Medical University, 1397-1 Yamane, Hidaka-shi, Saitama 350-1241, Japan
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Abstract
Chromosomal translocation product, TLS-CHOP (Translocated in liposarcoma-CCAAT/enhancer binding protein homologous protein, also named as FUS-DDIT3), has been thought to be a primary cause of myxoid liposarcoma, but the precise molecular function of TLS-CHOP for oncogenesis still remains to be elucidated. Previously we demonstrated that TLS/FUS interacts with protein arginine methyltransferase 1 (PRMT1), and carboxyl-terminal region of TLS is dimethylated by PRMT1. However, it has been uncovered whether TLS-CHOP function is regulated by PRMT1, and is methylated. Here we indicate that TLS-CHOP is not associated with PRMT1 and less methylated even though TLS-CHOP still possesses several potential arginine methylation sites of TLS. Moreover, we established a stable cell line expressing TLS-CHOP as a model system for studying the molecular function of TLS-CHOP. The TLS-CHOP expressing 293T cells exhibited slight growth retardation and decreased level of integrin 51 protein, a fibronectin receptor. It would be possible that the expression of oncoprotein TLS-CHOP might dysregulate arginine-specific methylation elicited via PRMT1 interacting with methylated TLS.
Keywords
TLS-CHOP, FUS-DDIT3, PRMT1, Arginine Methylation, Liposarcoma
To cite this article
Kenta Fujimoto, Shigeki Arai, Maki Matsubara, Kun Du, Yasuto Araki, Akio Matsushita, Riki Kurokawa, Implicated Role of Liposarcoma Related Fusion Oncoprotein TLS-CHOP in the Dysregulation of Arginine-Specific Methylation through PRMT1, Cell Biology. Vol. 1, No. 2, 2013, pp. 18-23. doi: 10.11648/j.cb.20130102.11
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