Evidence map›Paper›PMID 22011530›Full record

ArticleMolecular cancer2011

Aurora-A inactivation causes mitotic spindle pole fragmentation by unbalancing microtubule-generated forces.

Italia A Asteriti, Maria Giubettini, Patrizia Lavia, Giulia Guarguaglini

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

42 citing papers in PubMed, 59 citations in OpenAlex.

  1. Phase II study of alisertib, a selective Aurora A kinase inhibitor, in relapsed and refractory aggressive B- and T-cell non-Hodgkin lymphomas.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2014
    Trial
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  6. Microtubule regulation in cancer cells.Frontiers in cell and developmental biology · 2025
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  13. Targeting cytoskeletal phosphorylation in cancer.Exploration of targeted anti-tumor therapy · 2021
    Review
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  16. Allosteric modulation of a human protein kinase with monobodies.Proceedings of the National Academy of Sciences of the United States of America · 2019
    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

4 authors at 2 institutions in 1 country.

Italia A AsteritiInstitute of Molecular Biology and Pathology, CNR National Research Council, c/o Department of Biology and Biotechnologies, Sapienza University of Rome, Via degli Apuli 4, Rome, Italy.
Maria Giubettini
Patrizia Lavia
Giulia Guarguaglini
National Research Council · ITSapienza University of Rome · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAurora-A is an oncogenic kinase playing well-documented roles in mitotic spindle organisation. We previously found that Aurora-A inactivation yields the formation of spindles with fragmented poles that can drive chromosome mis-segregation. Here we have addressed the mechanism through which Aurora-A activity regulates the structure and cohesion of spindle poles.

resultsWe inactivated Aurora-A in human U2OS osteosarcoma cells either by RNA-interference-mediated silencing or treating cultures with the specific inhibitor MLN8237. We show that mitotic spindle pole fragmentation induced by Aurora-A inactivation is associated with microtubule hyperstabilisation. Silencing of the microtubule-stabilising factor ch-TOG prevents spindle pole fragmentation caused by inactivation of Aurora-A alone and concomitantly reduces the hyperstabilisation of microtubules. Furthermore, decreasing pole-directed spindle forces by inhibition of the Eg5 kinesin, or by destabilisation of microtubule-kinetochore attachments, also prevents pole fragmentation in Aurora-A-inactivated mitoses.

conclusionsOur findings indicate that microtubule-generated forces are imbalanced in Aurora-A-defective cells and exert abnormal pressure at the level of spindle poles, ultimately causing their fragmentation. This study therefore highlights a novel role of the Aurora-A kinase in regulating the balance between microtubule forces during bipolar spindle assembly.

Indexed as

Aurora KinasesAzepinesHumansKinesinsKinetochoresMicrotubulesProtein Kinase InhibitorsProtein Serine-Threonine KinasesPyrimidinesRNA InterferenceSpindle ApparatusTumor Cells, CulturedAurora KinasesAzepinesKIF11 protein, humanKinesinsMLN 8237Protein Kinase InhibitorsProtein Serine-Threonine KinasesPyrimidines

Identifiers

PMID22011530
PMCPMC3226445
OpenAlexW2171734408

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.