Evidence map›Paper›PMID 26943585›Full record

ArticleOncotarget2016

Novel Mad2-targeting miR-493-3p controls mitotic fidelity and cancer cells' sensitivity to paclitaxel.

Mahesh Tambe, Sofia Pruikkonen, Jenni Mäki-Jouppila, Ping Chen, Bente Vilming Elgaaen, Anne Hege Straume, Kaisa Huhtinen, Olli Cárpen, Per Eystein Lønning, Ben Davidson and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.2field-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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
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  10. Mitotic checkpoint defects: en route to cancer and drug resistance.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2021
    Review
  11. Article
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  13. Meiotic spindle assembly checkpoint and aneuploidy in males versus females.Cellular and molecular life sciences : CMLS · 2019
    Review
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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 7 institutions in 2 countries.

Mahesh TambeDepartment of Physiology, Institute of Biomedicine, University of Turku, Turku, Finland.
Sofia PruikkonenDepartment of Physiology, Institute of Biomedicine, University of Turku, Turku, Finland.
Jenni Mäki-JouppilaDepartment of Physiology, Institute of Biomedicine, University of Turku, Turku, Finland.
Ping ChenResearch Programs Unit, Genome-Scale Biology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Bente Vilming ElgaaenDepartment of Gynecological Oncology, Oslo University Hospital, Norwegian Radium Hospital, Oslo, Norway.
Anne Hege StraumeDepartment of Clinical Science, University of Bergen and Department of Clinical Oncology, Haukeland University Hospital, Bergen, Norway.
Kaisa HuhtinenDepartment of Pathology, University of Turku and Turku University Hospital, Turku, Finland.
Olli CárpenDepartment of Pathology, University of Turku and Turku University Hospital, Turku, Finland.
Per Eystein LønningDepartment of Clinical Science, University of Bergen and Department of Clinical Oncology, Haukeland University Hospital, Bergen, Norway.
Ben DavidsonDepartment of Pathology, Oslo University Hospital, Norwegian Radium Hospital, Oslo, Norway.
Sampsa HautaniemiResearch Programs Unit, Genome-Scale Biology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Marko J KallioDepartment of Physiology, Institute of Biomedicine, University of Turku, Turku, Finland.
University of Turku · FITurku Centre for Biotechnology · FIUniversity of Helsinki · FIHaukeland University Hospital · NOOslo University Hospital · NOUniversity of Bergen · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The molecular pathways that contribute to the proliferation and drug response of cancer cells are highly complex and currently insufficiently characterized. We have identified a previously unknown microRNA-based mechanism that provides cancer cells means to stimulate tumorigenesis via increased genomic instability and, at the same time, evade the action of clinically utilized microtubule drugs. We demonstrate miR-493-3p to be a novel negative regulator of mitotic arrest deficient-2 (MAD2), an essential component of the spindle assembly checkpoint that monitors the fidelity of chromosome segregation. The microRNA targets the 3' UTR of Mad2 mRNA thereby preventing translation of the Mad2 protein. In cancer cells, overexpression of miR-493-3p induced a premature mitotic exit that led to increased frequency of aneuploidy and cellular senescence in the progeny cells. Importantly, excess of the miR-493-3p conferred resistance of cancer cells to microtubule drugs. In human neoplasms, miR-493-3p and Mad2 expression alterations correlated with advanced ovarian cancer forms and high miR-493-3p levels were associated with reduced survival of ovarian and breast cancer patients with aggressive tumors, especially in the paclitaxel therapy arm. Our results suggest that intratumoral profiling of miR-493-3p and Mad2 levels can have diagnostic value in predicting the efficacy of taxane chemotherapy.

Indexed as

Breast NeoplasmsChromosome SegregationFemaleHCT116 CellsHeLa CellsHumansMad2 ProteinsMicroRNAsMitosisM Phase Cell Cycle CheckpointsNeoplasmsOvarian NeoplasmsPaclitaxelRandomized Controlled Trials as TopicTransfectionMAD2L1 protein, humanMad2 ProteinsMicroRNAsMIRN493 microRNA, humanPaclitaxelaneuploidyChromosome SectionMad2miR-493-3pspindle assembly checkpointtaxane resistance

Identifiers

PMID26943585
PMCPMC4914283
OpenAlexW2302397808

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.