Evidence map›Paper›PMID 12897130›Full record

ArticleMolecular and cellular biology2003

Silencing of the novel p53 target gene Snk/Plk2 leads to mitotic catastrophe in paclitaxel (taxol)-exposed cells.

Timothy F Burns, Peiwen Fei, Kimberly A Scata, David T Dicker, Wafik S El-Deiry

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

104 citing papers in PubMed, 224 citations in OpenAlex.

  1. Article
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  11. Journal of gastric cancer · 2022
    Article
  12. Review
  13. Mechanisms of cancer cell death induction by paclitaxel: an updated review.Apoptosis : an international journal on programmed cell death · 2022
    Review
  14. Article
  15. Article
  16. Review
  17. Reviewing cancer's biology: an eclectic approach.Journal of the Egyptian National Cancer Institute · 2021
    Review
  18. Review
  19. Review
  20. Article

44 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

5 authors at 3 institutions in 1 country.

Timothy F BurnsLaboratory of Molecular Oncology and Cell Cycle Regulation, Howard Hughes Medical Institute, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.
Peiwen Fei
Kimberly A Scata
David T Dicker
Wafik S El-Deiry
University of Pennsylvania · USHoward Hughes Medical Institute · USMolecular Oncology (United States) · US

Funding

ROLE OF ATAXIA TELANGIECTASIA IN CHECKPOINT CONTROLP01CA075138 · NCI · UNIVERSITY OF PENNSYLVANIA · PI HAHN, STEPHEN M · 1998 to 2007
$11.6M
RADIATION BIOLOGY TRAINING GRANTT32CA009677 · NCI · UNIVERSITY OF PENNSYLVANIA · PI KENNEDY, ANN R · 1992 to 2011
$5.0M
NCI NIH HHS P01 CA075138NCI NIH HHS P01 CA75138NCI NIH HHS T32 CA009677NCI NIH HHS T32 CA09677
6 · The paper itself

Abstract

Loss of p53 sensitizes to antimicrotubule agents in human tumor cells, but little is known about its role during mitosis. We have identified the Polo-like kinase family member serum inducible kinase (Snk/Plk2) as a novel p53 target gene. Snk/Plk2 mutagenesis demonstrated that its kinase activity is negatively regulated by its C terminus. Small interfering RNA (siRNA)-mediated Snk/Plk2 silencing in the presence of the mitotic poisons paclitaxel (Taxol) or nocodazole significantly increased apoptosis, similar to p53 mutations, which confer paclitaxel sensitivity. Furthermore, we have demonstrated that the apoptosis due to silencing of Snk/Plk2 in the face of spindle damage occurs in mitotic cells and not in cells that have progressed to a G(1)-like state without dividing. Since siRNA directed against Snk/Plk2 promoted death of paclitaxel-treated cells in mitosis, we envision a mitotic checkpoint wherein p53-dependent activation of Snk/Plk2 prevents mitotic catastrophe following spindle damage. Finally, these studies suggest that disruption of Snk/Plk2 may be of therapeutic value in sensitizing paclitaxel-resistant tumors.

Indexed as

Gene SilencingGenes, p53MitosisAnimalsAntineoplastic Agents, PhytogenicApoptosisBase SequenceBlotting, NorthernBlotting, WesternCell DeathCell LineChromatinDNA DamageDose-Response Relationship, RadiationFemaleFlow CytometryAntineoplastic Agents, PhytogenicChromatinGreen Fluorescent ProteinsLuciferasesLuminescent ProteinsPaclitaxelRNARNA, MessengerRNA, Small InterferingSerine EndopeptidasesTranscription Factors

Identifiers

PMID12897130
PMCPMC166320
OpenAlexW2170002512

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.