Evidence map›Paper›PMID 29549256›Full record

ArticleNature communications2018

PLK1 has tumor-suppressive potential in APC-truncated colon cancer cells.

Monika Raab, Mourad Sanhaji, Yves Matthess, Albrecht Hörlin, Ioana Lorenz, Christina Dötsch, Nils Habbe, Oliver Waidmann, Elisabeth Kurunci-Csacsko, Ron Firestein and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 66 citations in OpenAlex.

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  12. Role of microRNA in colorectal carcinoma (CRC): a narrative review.Annals of medicine and surgery (2012) · 2024
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  13. Review
  14. Kelch-like proteins in the gastrointestinal tumors.Acta pharmacologica Sinica · 2023
    Review
  15. Article
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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

12 authors at 3 institutions in 2 countries.

Monika RaabDepartment of Gynecology, Goethe-University, 60590, Frankfurt, Germany.
Mourad SanhajiDepartment of Gynecology, Goethe-University, 60590, Frankfurt, Germany.
Yves MatthessDepartment of Gynecology, Goethe-University, 60590, Frankfurt, Germany.
Albrecht HörlinInstitute of Pathology at the Department of Pathology, Goethe-University, 60590, Frankfurt, Germany.
Ioana LorenzDepartment of Gynecology, Goethe-University, 60590, Frankfurt, Germany.
Christina DötschDepartment of Gynecology, Goethe-University, 60590, Frankfurt, Germany.
Nils HabbeDepartment of General and Visceral Surgery, Goethe-University, 60590, Frankfurt, Germany.
Oliver WaidmannDepartment of Gastroenterology and Hepatology, Goethe-University, 60590, Frankfurt, Germany.
Elisabeth Kurunci-CsacskoDepartment of Gynecology, Goethe-University, 60590, Frankfurt, Germany.
Ron FiresteinCentre for Cancer Research, Hudson Institute of Medical Research, Clayton, AU 31681, Australia.
Sven BeckerDepartment of Gynecology, Goethe-University, 60590, Frankfurt, Germany.
Klaus StrebhardtDepartment of Gynecology, Goethe-University, 60590, Frankfurt, Germany. strebhardt@em.uni-frankfurt.de.
Goethe University Frankfurt · DEHeidelberg University · DEHudson Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The spindle assembly checkpoint (SAC) acts as a molecular safeguard in ensuring faithful chromosome transmission during mitosis, which is regulated by a complex interplay between phosphatases and kinases including PLK1. Adenomatous polyposis coli (APC) germline mutations cause aneuploidy and are responsible for familial adenomatous polyposis (FAP). Here we study the role of PLK1 in colon cancer cells with chromosomal instability promoted by APC truncation (APC-ΔC). The expression of APC-ΔC in colon cells reduces the accumulation of mitotic cells upon PLK1 inhibition, accelerates mitotic exit and increases the survival of cells with enhanced chromosomal abnormalities. The inhibition of PLK1 in mitotic, APC-∆C-expressing cells reduces the kinetochore levels of Aurora B and hampers the recruitment of SAC component suggesting a compromised mitotic checkpoint. Furthermore, Plk1 inhibition (RNAi, pharmacological compounds) promotes the development of adenomatous polyps in two independent Apc

Indexed as

Adenomatous Polyposis ColiAdenomatous Polyposis Coli ProteinAnimalsAurora Kinase BCell Cycle ProteinsCell Line, TumorChromosomal InstabilityColonic NeoplasmsFemaleHumansKinetochoresMaleMiceMice, Inbred C57BLMice, KnockoutMitosisAdenomatous Polyposis Coli ProteinAurora Kinase BCell Cycle ProteinsPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsTumor Suppressor Proteins

Identifiers

PMID29549256
PMCPMC5856809
OpenAlexW2791171259

What OpenQuestion holds

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LicenceCC BY
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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.