PRMT1 promotes mitosis of cancer cells through arginine methylation of INCENP

Inner centromere protein (INCENP) is a part of a protein complex known as the chromosomal passenger complex (CPC) that is essential for correcting non-bipolar chromosome attachments and for cytokinesis. We here demonstrate that a protein arginine methyltransferase PRMT1, which are overexpressed in v...

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Bibliographic Details
Published in:Oncotarget 2015-11, Vol.6 (34), p.35173-35182
Main Authors: Deng, Xiaolan, Von Keudell, Gottfried, Suzuki, Takehiro, Dohmae, Naoshi, Nakakido, Makoto, Piao, Lianhua, Yoshioka, Yuichiro, Nakamura, Yusuke, Hamamoto, Ryuji
Format: Article
Language:English
Subjects:
Amino Acid Sequence
Arginine - metabolism
Cell Line, Tumor
Chromosomal Proteins, Non-Histone - metabolism
HEK293 Cells
HeLa Cells
Humans
Methylation
Mitosis - physiology
Molecular Sequence Data
Neoplasms - enzymology
Neoplasms - metabolism
Neoplasms - pathology
Priority Research Paper
Protein-Arginine N-Methyltransferases - metabolism
Repressor Proteins - metabolism
Transfection
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Summary:Inner centromere protein (INCENP) is a part of a protein complex known as the chromosomal passenger complex (CPC) that is essential for correcting non-bipolar chromosome attachments and for cytokinesis. We here demonstrate that a protein arginine methyltransferase PRMT1, which are overexpressed in various types of cancer including lung and bladder cancer, methylates arginine 887 in an Aurora Kinase B (AURKB)-binding region of INCENP both in vitro and in vivo. R887-substituted INCENP revealed lower binding-affinity to AURKB than wild-type INCENP in the presence of PRMT1. Knockdown of PRMT1 as well as overexpression of methylation-inactive INCENP attenuated the AURKB activity in cancer cells, and resulted in abnormal chromosomal alignment and segregation. Furthermore, introduction of methylation-inactive INCENP into cancer cells reduced the growth rate, compared with those introduced wild-type INCENP or Mock. Our data unveils a novel mechanism of PRMT1-mediated CPC regulation through methylation of INCENP.
ISSN:1949-2553
1949-2553
DOI:10.18632/oncotarget.6050