Evidence map›Paper›PMID 24101154›Full record

ArticleCancer research2013

CDK1 phosphorylation of YAP promotes mitotic defects and cell motility and is essential for neoplastic transformation.

Shuping Yang, Lin Zhang, Miao Liu, Rong Chong, Shi-Jian Ding, Yuanhong Chen, Jixin Dong

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

79 citing papers in PubMed, 128 citations in OpenAlex.

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  18. Optogenetic control of YAP can enhance the rate of wound healing.Cellular & molecular biology letters · 2023
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  20. Article

19 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Shuping YangAuthors' Affiliations: Eppley Institute for Research in Cancer and Allied Diseases; Department of Pathology and Microbiology; and Mass Spectrometry and Proteomics Core Facility, University of Nebraska Medical Center, Omaha, Nebraska.
Lin Zhang
Miao Liu
Rong Chong
Shi-Jian Ding
Yuanhong Chen
Jixin Dong
University of Nebraska Medical Center · US

Funding

SUPPRESSIVE ROLE OF TGFBETA IN METASTASIS OF COLON CANCERP20RR018759 · NCRR · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI JOHNSON, KEITH R · 2003 to 2011
$17.9M
Nebraska Center for Cellular SignalingP20GM103489 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI JOHNSON, KEITH R · 2012 to 2012
$2.0M
Regulation and Functional Dissection of YAP in MitosisR01GM109066 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI DONG, JIXIN · 2014 to 2018
$1.4M
NCRR NIH HHS P20 RR018759NIGMS NIH HHS 8P20 GM103489NIGMS NIH HHS P20 GM103489NIGMS NIH HHS R01 GM109066
6 · The paper itself

Abstract

The Yes-associated protein, YAP, is a downstream effector of the Hippo pathway of cell-cycle control that plays important roles in tumorigenesis. Hippo-mediated phosphorylation YAP, mainly at S127, inactivates YAP function. In this study, we define a mechanism for positive regulation of YAP activity that is critical for its oncogenic function. Specifically, we found that YAP is phosphorylated in vitro and in vivo by the cell-cycle kinase CDK1 at T119, S289, and S367 during the G2-M phase of the cell cycle. We also found that ectopic expression of a phosphomimetic YAP mutant (YAP3D, harboring T119D/S289D/S367D) was sufficient to induce mitotic defects in immortalized epithelial cells, including centrosome amplification, multipolar spindles, and chromosome missegregation. Finally, we documented that mitotic phosphorylation of YAP was sufficient to promote cell migration and invasion in a manner essential for neoplastic cell transformation. In support of our findings, CDK1 inhibitors largely suppressed cell motility mediated by activated YAP-S127A but not the phosphomimetic mutant YAP3D. Collectively, our results reveal a previously unrecognized mechanism for controlling the activity of YAP that is crucial for its oncogenic function mediated by mitotic dysregulation.

Indexed as

Cell MovementMitosisAntineoplastic AgentsBinding SitesCDC2 Protein KinaseCell Cycle ProteinsCells, CulturedCell Transformation, NeoplasticHCT116 CellsHEK293 CellsHeLa CellsHumansMCF-7 CellsNocodazoleNuclear ProteinsPaclitaxelAntineoplastic AgentsCDC2 Protein KinaseCell Cycle ProteinsNocodazoleNuclear ProteinsPaclitaxelTranscription FactorsYY1AP1 protein, human

Identifiers

PMID24101154
PMCPMC3861241
OpenAlexW2116231448

What OpenQuestion holds

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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.