Evidence map›Paper›PMID 25174401›Full record

ArticleOncogene2015

A novel role for Plk4 in regulating cell spreading and motility.

C O Rosario, K Kazazian, F S W Zih, O Brashavitskaya, Y Haffani, R S Z Xu, A George, J W Dennis, C J Swallow

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

36 citing papers in PubMed, 65 citations in OpenAlex.

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  4. DysregulatedLife science alliance · 2025
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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

9 authors at 3 institutions in 1 country.

C O Rosario1] Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada [2] Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.
K Kazazian1] Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada [2] Department of Surgery, University of Toronto, Toronto, ON, Canada [3] Institute of Medical Science, University of Toronto, Toronto, ON, Canada.
F S W Zih1] Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada [2] Department of Surgery, University of Toronto, Toronto, ON, Canada [3] Institute of Medical Science, University of Toronto, Toronto, ON, Canada.
O Brashavitskaya1] Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada [2] Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.
Y HaffaniLunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada.
R S Z Xu1] Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada [2] Institute of Medical Science, University of Toronto, Toronto, ON, Canada.
A GeorgeLunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada.
J W Dennis1] Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada [2] Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada [3] Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada.
C J Swallow1] Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada [2] Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada [3] Department of Surgery, University of Toronto, Toronto, ON, Canada [4] Institute of Medical Science, University of Toronto, Toronto, ON, Canada.
Mount Sinai Hospital · CALunenfeld-Tanenbaum Research Institute · CAUniversity of Toronto · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Polo family kinase 4 (Plk4) is required for mitotic progression, and is haploinsufficient for tumor suppression and timely hepatocyte polarization in regenerating liver. At the same time, recent evidence suggests that Plk4 expression may have a role in clinical cancer progression, although the mechanisms are not clear. Here we identify a gene expression pattern predictive of reduced motility in Plk4(+/-) murine embryonic fibroblasts (MEFs) and validate this prediction with functional assays of cell spreading, migration and invasion. Increased Plk4 expression enhances cell spreading in Plk4(+/-) MEFs and migration in human embryonic kidney 293T cells, and increases invasion by DLD-1 colon cancer cells. Plk4 depletion impairs invasion of wild-type MEFs and suppresses invasion by MDA-MB231 breast cancer cells. Cytoskeletal reorganization and development of polarity are impaired in Plk4-deficient cells that have been stimulated to migrate. Endogenous Plk4 phosphorylated at the autophosphorylation site S305 localizes to the protrusions of motile cells, coincident with the RhoA GEF Ect2, GTP-bound RhoA and the RhoA effector mDia. Taken together, our findings reveal an unexpected activity of Plk4 that promotes cell migration and may underlie an association between increased Plk4 expression, cancer progression and death from metastasis in solid tumor patients.

Indexed as

AnimalsCell AdhesionCell MovementCell ProliferationCells, CulturedDisease ProgressionEmbryo, MammalianHEK293 CellsHeLa CellsHumansMiceMice, Inbred NODMice, SCIDNeoplasm MetastasisNeoplasmsProtein Serine-Threonine KinasesPLK4 protein, humanProtein Serine-Threonine Kinases

Identifiers

PMID25174401
OpenAlexW2074897052

What OpenQuestion holds

Textmetadata
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.