Implicated Role of Liposarcoma Related Fusion Oncoprotein TLS-CHOP in the Dysregulation of Arginine-Specific Methylation through PRMT1

Kenta Fujimoto; Shigeki Arai; Maki Matsubara; Kun Du; Yasuto Araki; Akio Matsushita; Riki Kurokawa

doi:doi:10.11648/j.cb.20130102.11

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Implicated Role of Liposarcoma Related Fusion Oncoprotein TLS-CHOP in the Dysregulation of Arginine-Specific Methylation through PRMT1

Kenta Fujimoto, Shigeki Arai, Maki Matsubara, Kun Du, Yasuto Araki, Akio Matsushita, Riki Kurokawa

Published in Cell Biology (Volume 1, Issue 2)

Received: 3 October 2013 Published: 10 December 2013

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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.

Published in	Cell Biology (Volume 1, Issue 2)
DOI	10.11648/j.cb.20130102.11
Page(s)	18-23
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2013. Published by Science Publishing Group

Keywords

TLS-CHOP, FUS-DDIT3, PRMT1, Arginine Methylation, Liposarcoma

References

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[13]	Kwiatkowski, T.J. et al. (2009). Mutations in the FUS/TLS gene on chromosome 16 cause familial amyotrophic lateral sclerosis. Science 323, 1205-1208.
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[23]	Nicholson, T.B., Chen, T. and Richard, S. (2009). The physiological and pathophysiological role of PRMT1-mediated protein arginine methylation. Pharmacol Res 60, 466-474.
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[25]	Plantefaber, L.C. and Hynes, R.O. (1989). Changes in integrin receptors on oncogenically transformed cells. Cell 56, 281-290.
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[27]	Thelin-Järnum, S., Göransson, M., Burguete, A.S., Olofsson, A. and Aman, P. (2002). The myxoid liposarcoma specific TLS-CHOP fusion protein localizes to nuclear structures distinct from PML nuclear bodies. Int J Cancer 97, 446-450.
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APA Style

Kenta Fujimoto, Shigeki Arai, Maki Matsubara, Kun Du, Yasuto Araki, et al. (2013). Implicated Role of Liposarcoma Related Fusion Oncoprotein TLS-CHOP in the Dysregulation of Arginine-Specific Methylation through PRMT1. Cell Biology, 1(2), 18-23. https://doi.org/10.11648/j.cb.20130102.11

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ACS Style

Kenta Fujimoto; Shigeki Arai; Maki Matsubara; Kun Du; Yasuto Araki, et al. Implicated Role of Liposarcoma Related Fusion Oncoprotein TLS-CHOP in the Dysregulation of Arginine-Specific Methylation through PRMT1. Cell Biol. 2013, 1(2), 18-23. doi: 10.11648/j.cb.20130102.11

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AMA Style

Kenta Fujimoto, Shigeki Arai, Maki Matsubara, Kun Du, Yasuto Araki, et al. Implicated Role of Liposarcoma Related Fusion Oncoprotein TLS-CHOP in the Dysregulation of Arginine-Specific Methylation through PRMT1. Cell Biol. 2013;1(2):18-23. doi: 10.11648/j.cb.20130102.11

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@article{10.11648/j.cb.20130102.11,
  author = {Kenta Fujimoto and Shigeki Arai and Maki Matsubara and Kun Du and Yasuto Araki and Akio Matsushita and Riki Kurokawa},
  title = {Implicated Role of Liposarcoma Related Fusion Oncoprotein TLS-CHOP in the Dysregulation of Arginine-Specific Methylation through PRMT1},
  journal = {Cell Biology},
  volume = {1},
  number = {2},
  pages = {18-23},
  doi = {10.11648/j.cb.20130102.11},
  url = {https://doi.org/10.11648/j.cb.20130102.11},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cb.20130102.11},
  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.},
 year = {2013}
}

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TY  - JOUR
T1  - Implicated Role of Liposarcoma Related Fusion Oncoprotein TLS-CHOP in the Dysregulation of Arginine-Specific Methylation through PRMT1
AU  - Kenta Fujimoto
AU  - Shigeki Arai
AU  - Maki Matsubara
AU  - Kun Du
AU  - Yasuto Araki
AU  - Akio Matsushita
AU  - Riki Kurokawa
Y1  - 2013/12/10
PY  - 2013
N1  - https://doi.org/10.11648/j.cb.20130102.11
DO  - 10.11648/j.cb.20130102.11
T2  - Cell Biology
JF  - Cell Biology
JO  - Cell Biology
SP  - 18
EP  - 23
PB  - Science Publishing Group
SN  - 2330-0183
UR  - https://doi.org/10.11648/j.cb.20130102.11
AB  - 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.
VL  - 1
IS  - 2
ER  -

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Author Information

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
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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APA Style

Kenta Fujimoto, Shigeki Arai, Maki Matsubara, Kun Du, Yasuto Araki, et al. (2013). Implicated Role of Liposarcoma Related Fusion Oncoprotein TLS-CHOP in the Dysregulation of Arginine-Specific Methylation through PRMT1. Cell Biology, 1(2), 18-23. https://doi.org/10.11648/j.cb.20130102.11

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ACS Style

Kenta Fujimoto; Shigeki Arai; Maki Matsubara; Kun Du; Yasuto Araki, et al. Implicated Role of Liposarcoma Related Fusion Oncoprotein TLS-CHOP in the Dysregulation of Arginine-Specific Methylation through PRMT1. Cell Biol. 2013, 1(2), 18-23. doi: 10.11648/j.cb.20130102.11

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AMA Style

Kenta Fujimoto, Shigeki Arai, Maki Matsubara, Kun Du, Yasuto Araki, et al. Implicated Role of Liposarcoma Related Fusion Oncoprotein TLS-CHOP in the Dysregulation of Arginine-Specific Methylation through PRMT1. Cell Biol. 2013;1(2):18-23. doi: 10.11648/j.cb.20130102.11

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@article{10.11648/j.cb.20130102.11,
  author = {Kenta Fujimoto and Shigeki Arai and Maki Matsubara and Kun Du and Yasuto Araki and Akio Matsushita and Riki Kurokawa},
  title = {Implicated Role of Liposarcoma Related Fusion Oncoprotein TLS-CHOP in the Dysregulation of Arginine-Specific Methylation through PRMT1},
  journal = {Cell Biology},
  volume = {1},
  number = {2},
  pages = {18-23},
  doi = {10.11648/j.cb.20130102.11},
  url = {https://doi.org/10.11648/j.cb.20130102.11},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cb.20130102.11},
  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.},
 year = {2013}
}

Copy | Download

TY  - JOUR
T1  - Implicated Role of Liposarcoma Related Fusion Oncoprotein TLS-CHOP in the Dysregulation of Arginine-Specific Methylation through PRMT1
AU  - Kenta Fujimoto
AU  - Shigeki Arai
AU  - Maki Matsubara
AU  - Kun Du
AU  - Yasuto Araki
AU  - Akio Matsushita
AU  - Riki Kurokawa
Y1  - 2013/12/10
PY  - 2013
N1  - https://doi.org/10.11648/j.cb.20130102.11
DO  - 10.11648/j.cb.20130102.11
T2  - Cell Biology
JF  - Cell Biology
JO  - Cell Biology
SP  - 18
EP  - 23
PB  - Science Publishing Group
SN  - 2330-0183
UR  - https://doi.org/10.11648/j.cb.20130102.11
AB  - 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.
VL  - 1
IS  - 2
ER  -

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