Evidence map›Paper›PMID 31358734›Full record

ArticleCell death & disease2019

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

Dong Hyun Kim, Jong Seog Ahn, Ho Jin Han, Hye-Min Kim, Joonsung Hwang, Kyung Ho Lee, Hyunjoo Cha-Molstad, In-Ja Ryoo, Jae-Hyuk Jang, Sung-Kyun Ko and 9 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.0field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 40 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors at 4 institutions in 2 countries.

Dong Hyun KimAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongju, 28116, Republic of Korea.ORCID http://orcid.org/0000-0002-7463-209X
Jong Seog AhnAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongju, 28116, Republic of Korea.
Ho Jin HanAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongju, 28116, Republic of Korea.
Hye-Min KimAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongju, 28116, Republic of Korea.
Joonsung HwangAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongju, 28116, Republic of Korea.
Kyung Ho LeeAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongju, 28116, Republic of Korea.
Hyunjoo Cha-MolstadAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongju, 28116, Republic of Korea.
In-Ja RyooAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongju, 28116, Republic of Korea.
Jae-Hyuk JangAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongju, 28116, Republic of Korea.ORCID http://orcid.org/0000-0002-4363-4252
Sung-Kyun KoAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongju, 28116, Republic of Korea.
Jin Ok YangKorean Bioinformation Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Republic of Korea.
Hee Gu LeeImmunotherapy Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Republic of Korea.
Sangku LeeAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongju, 28116, Republic of Korea.
Eun Joo SongMolecular Recognition Research Center, Korea Institute of Science and Technology, Seoul, 02792, Republic of Korea.ORCID http://orcid.org/0000-0002-2420-6666
Jin Young KimBiomedical Omics Research, Korea Basic Science Institute, Ochang, Cheongju, 28119, Republic of Korea.
Yang Hoon HuhCenter for Electron Microscopy Research, Korea Basic Science Institute, Ochang, Cheongju, 28119, Republic of Korea.
Yong Tae KwonProtein Metabolism Medical Research Center, Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Republic of Korea. yok5@snu.ac.kr.
Nak-Kyun SoungAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongju, 28116, Republic of Korea. soungnak@kribb.re.kr.ORCID http://orcid.org/0000-0002-7325-308X
Bo Yeon KimAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongju, 28116, Republic of Korea. bykim@kribb.re.kr.ORCID http://orcid.org/0000-0003-1105-5480
Korea Research Institute of Bioscience and Biotechnology · KRKorea Basic Science Institute · KRKorea Institute of Science and Technology · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AnimalsCell Cycle ProteinsCell Line, TumorCentrosomeColonic NeoplasmsCytoskeletal ProteinsDisease ProgressionGene Expression Regulation, NeoplasticHCT116 CellsHEK293 CellsHeterograftsHumansIntracellular Signaling Peptides and ProteinsMicePhosphorylationProtein Serine-Threonine KinasesCell Cycle ProteinsCEP131 protein, humanCytoskeletal ProteinsIntracellular Signaling Peptides and ProteinsPLK4 protein, humanProtein Serine-Threonine KinasesSTIL protein, human

Identifiers

PMID31358734
PMCPMC6662699
OpenAlexW2965492852

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.