Cep131 overexpression promotes centrosome amplification and colon cancer progression by regulating Plk4 stability

Cited 8 time in scopus
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Title
Cep131 overexpression promotes centrosome amplification and colon cancer progression by regulating Plk4 stability
Author(s)
Dong Hyun Kim; Jong Seog Ahn; Ho Jin Han; Hye-Min Kim; Joonsung HwangKyung Ho LeeHyunjoo ChaIn Ja RyooJae-Hyuk JangSung-Kyun KoJin Ok YangHee Gu LeeSangku Lee; E J Song; J Y Kim; Y H Huh; Y T Kwon; Nak Kyun SoungBo Yeon Kim
Bibliographic Citation
Cell Death & Disease, vol. 10, no. 8, pp. 570-570
Publication Year
2019
Abstract
The initiation of centrosome duplication is regulated by the Plk4/STIL/hsSAS-6 axis; however, the involvement of other centrosomal proteins in this process remains unclear. In this study, we demonstrate that Cep131 physically interacts with Plk4 following phosphorylation of residues S21 and T205. Localizing at the centriole, phosphorylated Cep131 has an increased capability to interact with STIL, leading to further activation and stabilization of Plk4 for initiating centrosome duplication. Moreover, we found that Cep131 overexpression resulted in centrosome amplification by excessive recruitment of STIL to the centriole and subsequent stabilization of Plk4, contributing to centrosome amplification. The xenograft mouse model also showed that both centrosome amplification and colon cancer growth were significantly increased by Cep131 overexpression. These findings demonstrate that Cep131 is a novel substrate of Plk4, and that phosphorylation or dysregulated Cep131 overexpression promotes Plk4 stabilization and therefore centrosome amplification, establishing a perspective in understanding a relationship between centrosome amplification and cancer development.
ISSN
2041-4889
Publisher
Springer-Nature Pub Group
DOI
http://dx.doi.org/10.1038/s41419-019-1778-8
Type
Article
Appears in Collections:
Ochang Branch Institute > Anticancer Agent Research Center > 1. Journal Articles
Ochang Branch Institute > Natural Medicine Research Center > 1. Journal Articles
Korea Bioinformation Center > 1. Journal Articles
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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