Evidence map›Paper›PMID 16027732›Full record

ArticleOncogene2005

Aurora-B/AIM-1 kinase activity is involved in Ras-mediated cell transformation.

Akifumi Kanda, Hidehiko Kawai, Shiho Suto, Shojiro Kitajima, Sunao Sato, Takashi Takata, Masaaki Tatsuka

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

32 citing papers in PubMed, 80 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Aurora B kinase: a potential drug target for cancer therapy.Journal of cancer research and clinical oncology · 2021
    Review
  7. Review
  8. Chiauranib selectively inhibits colorectal cancer withAmerican journal of cancer research · 2020
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. A new aurora in anaplastic thyroid cancer therapy.International journal of endocrinology · 2014
    Review
  17. Review
  18. Review
  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

7 authors at 1 institution in 1 country.

Akifumi KandaDepartment of Molecular Radiobiology, Division of Genome Biology, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734, Japan.
Hidehiko Kawai
Shiho Suto
Shojiro Kitajima
Sunao Sato
Takashi Takata
Masaaki Tatsuka
Hiroshima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aurora-B, previously known as AIM-1, is a conserved eukaryotic mitotic protein kinase. In mammals, this kinase plays an essential role in chromosomal segregation processes, including chromosome condensation, alignment, control of spindle checkpoints, chromosome segregation, and cytokinesis. Aurora-B is overexpressed in various cancer cells, suggesting that the kinase activity perturbs chromosomal segregation processes. Its forced overexpression induces chromosomal number instability and progressive tumorigenicity in rodent cells in vitro and in vivo. Nevertheless, based on focus formation in BALB/c 3T3 A31-1-1 cells, Aurora-B is not oncogenic. Here, we show that Aurora-B kinase activity augments Ras-mediated cell transformation. RNA interference with short hairpin RNA inhibits transformation by Ras and its upstream oncogene Src, but not by the downstream oncogene Raf. In addition, the inner centromere protein, which is a passenger protein associated with Aurora-B, has a similar ability to potentiate the activity of oncogenic Ras. These data indicate that elevated Aurora-B activity promotes transformation by oncogenic Ras by enhancing oncogenic signaling and by converting chromosome number-stable cells to aneuploid cells.

Indexed as

AneuploidyAnimalsAntineoplastic AgentsAurora Kinase BAurora KinasesBALB 3T3 CellsCell Transformation, NeoplasticChromosomal Proteins, Non-HistoneGenes, rasGenes, srcMiceNocodazoleProtein Serine-Threonine Kinasesraf KinasesRNA InterferenceAntineoplastic AgentsAurkb protein, mouseAurora Kinase BAurora KinasesChromosomal Proteins, Non-HistoneIncenp protein, mouseNocodazoleProtein Serine-Threonine Kinasesraf Kinases

Identifiers

PMID16027732
OpenAlexW2049341882

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.