Evidence map›Paper›PMID 16630117›Full record

ArticleCancer science2006

Wilms' tumor gene WT1 17AA(-)/KTS(-) isoform induces morphological changes and promotes cell migration and invasion in vitro.

Tanyarat Jomgeow, Yusuke Oji, Naoko Tsuji, Yoko Ikeda, Ken Ito, Asako Tsuda, Tsutomu Nakazawa, Naoya Tatsumi, Nao Sakaguchi, Satoshi Takashima and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer science, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

33 citing papers in PubMed, 71 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Identification of mouse helper epitopes for WT1-specific CD4Cancer immunology, immunotherapy : CII · 2021
    Article
  9. Article
  10. Wilms' tumor 1 (Cell cycle (Georgetown, Tex.) · 2020
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Understanding CD8Clinical & translational immunology · 2017
    Article
  18. Article
  19. Review
  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

18 authors at 3 institutions in 2 countries.

Tanyarat JomgeowDepartment of Functional Diagnostic Science, Osaka University Graduate School of Medicine, 1-7 Yamada-oka, Suita, Osaka 565-0871, Japan.
Yusuke Oji
Naoko Tsuji
Yoko Ikeda
Ken Ito
Asako Tsuda
Tsutomu Nakazawa
Naoya Tatsumi
Nao Sakaguchi
Satoshi Takashima
Toshiaki Shirakata
Sumiyuki Nishida
Naoki Hosen
Manabu Kawakami
Akihiro Tsuboi
Yoshihiro Oka
Kazuyuki Itoh
Haruo Sugiyama
The University of Osaka · JPInstitute of Molecular Medicine · INOsaka International Cancer Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The wild-type Wilms' tumor gene WT1 is overexpressed in human primary leukemia and in a wide variety of solid cancers. All of the four WT1 isoforms are expressed in primary cancers and each is considered to have a different function. However, the functions of each of the WT1 isoforms in cancer cells remain unclear. The present study demonstrated that constitutive expression of the WT1 17AA(-)/KTS(-) isoform induces morphological changes characterized by a small-sized cell shape in TYK-nu.CP-r (TYK) ovarian cancer cells. In the WT1 17AA(-)/KTS(-) isoform-transduced TYK cells, cell-substratum adhesion was suppressed, and cell migration and in vitro invasion were enhanced compared to that in mock vector-transduced TYK cells. Constitutive expression of the WT1 17AA(-)/KTS(-) isoform also induced morphological changes in five (one gastric, one esophageal, two breast and one fibrosarcoma) of eight cancer cell lines examined. No WT1 isoforms other than the WT1 17AA(-)/KTS(-) isoform induced the phenotypic changes. A decrease in alpha-actinin 1 and cofilin expression and an increase in gelsolin expression were observed in WT1 17AA(-)/KTS(-) isoform-transduced TYK cells. In contrast, co-expression of alpha-actinin 1 and cofilin or knockdown of gelsolin expression by small interfering RNA restored WT1 17AA(-)/KTS(-) isoform-transduced TYK cells to a phenotype that was comparable to that of the parent TYK cells. These results indicated that the WT1 17AA(-)/KTS(-) isoform exerted its oncogenic functions through modulation of cytoskeletal dynamics. The present results may provide a novel insight into the signaling pathway of the WT1 gene for its oncogenic functions.

Indexed as

Cell MovementNeoplasm InvasivenessActininBlotting, WesternCell AdhesionCell SizeGelsolinGenes, Wilms TumorGenetic VectorsHumansIn Vitro TechniquesNeoplasmsProtein IsoformsReverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingTumor Cells, CulturedActininGelsolinProtein IsoformsRNA, Small InterferingWT1 Proteins

Identifiers

PMID16630117
PMCPMC11160036
OpenAlexW1769953224

What OpenQuestion holds

Textmetadata
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.