PRMT1 promotes mitosis of cancer cells through arginine methylation of INCENP
By Xiaolan Deng, Gottfried von Keudell, Takehiro Suzuki, N. Dohmae, Makoto Nakakido, Lianhua Piao, Yuichiro Yoshioka, Yusuke Nakamura, Ryuji Hamamoto. 2015
36 citations recorded by the source corpus.
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.
Subfields: Molecular Biology
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In Molecular Biology
- Ryuji Hamamoto
- Takehiro Suzuki
- N. Dohmae
- Yusuke Nakamura
- Yuichiro Yoshioka
- Y. Matsuo
- Toshiaki Watanabe
- G. Tsurita
Citations in the corpus
- Protein lysine methyltransferase SMYD3 is involved in tumorigenesis through regulation of HER2 homodimerization (2017, methodology): “Eluted samples were boiled with Lane Marker Sample Buffer (Thermo Fisher Scientific), and used for western blot analysis. siRNA transfection and cell growth assay siRNA oligonucleotide duplexes were purchased from Sigma- Aldrich for targeting the human SMYD3 transcripts (SASI Hs01_00188121 and SASI ”