Evidence map›Paper›PMID 15378001›Full record

ArticleOncogene2004

Cyclin-dependent kinase inhibitor indirubin-3'-oxime selectively inhibits human papillomavirus type 16 E7-induced numerical centrosome anomalies.

Stefan Duensing, Anette Duensing, David C Lee, Kirsten M Edwards, Siribang-On Piboonniyom, Edwin Manuel, Leandros Skaltsounis, Laurent Meijer, Karl Münger

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Centrosome amplification, chromosomal instability and cancer: mechanistic, clinical and therapeutic issues.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2016
    Review
  6. Article
  7. Indirubin and Indirubin Derivatives for Counteracting Proliferative Diseases.Evidence-based complementary and alternative medicine : eCAM · 2015
    Review
  8. Increased radiosensitivity of HPV-positive head and neck cancer cell lines due to cell cycle dysregulation and induction of apoptosis.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2014
    Article
  9. Review
  10. Article
  11. A clinical overview of centrosome amplification in human cancers.International journal of biological sciences · 2011
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Human papilloma virus (HPV) and host cellular interactions.Pathology oncology research : POR · 2008
    Review
  17. Article
  18. Article
  19. Article
  20. Article
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 5 institutions in 3 countries.

Stefan DuensingMolecular Virology Program, University of Pittsburgh Cancer Institute, Hillman Cancer Center, 5117 Centre Avenue, Pittsburgh, PA 15213, USA.
Anette Duensing
David C Lee
Kirsten M Edwards
Siribang-On Piboonniyom
Edwin Manuel
Leandros Skaltsounis
Laurent Meijer
Karl Münger
Harvard University · USCentre National de la Recherche Scientifique · FRNational and Kapodistrian University of Athens · GRUniversity of Pittsburgh · USUPMC Hillman Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation of the centrosome duplication cycle has been implicated in tumorigenesis. Our previous work has shown that the human papillomavirus type 16 (HPV-16) E7 oncoprotein rapidly induces aberrant centrosome and centriole duplication in normal human cells. We report here that HPV E7-induced abnormal centriole duplication is specifically abrogated by a small molecule CDK inhibitor, indirubin-3'-oxime (IO), but not a kinase-inactive derivative. Importantly, normal centriole duplication was not markedly affected by IO, and the inhibitory effects were observed at concentrations that did not affect the G1/S transition of the cell division cycle. Depletion of CDK2 by siRNA similarly abrogated HPV E7-induced abnormal centrosome duplication and ectopic expression of CDK2 in combination with cyclin E or cyclin A could rescue the inhibitory effect of IO. IO treatment also reduced the steady-state level of aneuploid cells in HPV-16 E7-expressing cell populations. Our results suggest that cyclin/CDK2 activity is critically involved in abnormal centrosome duplication induced by HPV-16 E7 oncoprotein expression, but may be dispensable for normal centrosome duplication and cell cycle progression.

Indexed as

CentrosomeBase SequenceCell Line, TumorCyclin-Dependent KinasesEnzyme InhibitorsHumansIndolesOncogene Proteins, ViralOximesPapillomavirus E7 ProteinsRNAS PhaseCyclin-Dependent KinasesEnzyme Inhibitorsindirubin-3'-monoximeIndolesoncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralOximesPapillomavirus E7 ProteinsRNA

Identifiers

PMID15378001
OpenAlexW2052428303

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.