Evidence map›Paper›PMID 22028615›Full record

ArticleNeoplasia (New York, N.Y.)2011

Histone lysine methyltransferase Wolf-Hirschhorn syndrome candidate 1 is involved in human carcinogenesis through regulation of the Wnt pathway.

Gouji Toyokawa, Hyun-Soo Cho, Ken Masuda, Yuka Yamane, Masanori Yoshimatsu, Shinya Hayami, Masashi Takawa, Yukiko Iwai, Yataro Daigo, Eiju Tsuchiya and 8 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

62 citing papers in PubMed, 99 citations in OpenAlex.

  1. Article
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  8. Review
  9. Review
  10. The role of NSD1, NSD2, and NSD3 histone methyltransferases in solid tumors.Cellular and molecular life sciences : CMLS · 2022
    Review
  11. Article
  12. Review
  13. Critical Roles ofBiomolecules · 2020
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

2 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

18 authors at 5 institutions in 2 countries.

Gouji ToyokawaLaboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Tokyo, Japan.
Hyun-Soo Cho
Ken Masuda
Yuka Yamane
Masanori Yoshimatsu
Shinya Hayami
Masashi Takawa
Yukiko Iwai
Yataro Daigo
Eiju Tsuchiya
Tatsuhiko Tsunoda
Helen I Field
John D Kelly
David E Neal
Yoshihiko Maehara
Bruce Aj Ponder
Yusuke Nakamura
Ryuji Hamamoto
The University of Tokyo · JPUniversity College London · GBUniversity of Cambridge · GBCancer Research UK · GBKanagawa Cancer Center

Funding

Cancer Research UK 19275
6 · The paper itself

Abstract

A number of histone methyltransferases have been identified and biochemically characterized, but the pathologic roles of their dysfunction in human diseases like cancer are not well understood. Here, we demonstrate that Wolf-Hirschhorn syndrome candidate 1 (WHSC1) plays important roles in human carcinogenesis. Transcriptional levels of this gene are significantly elevated in various types of cancer including bladder and lung cancers. Immunohistochemical analysis using a number of clinical tissues confirmed significant up-regulation of WHSC1 expression in bladder and lung cancer cells at the protein level. Treatment of cancer cell lines with small interfering RNA targeting WHSC1 significantly knocked down its expression and resulted in the suppression of proliferation. Cell cycle analysis by flow cytometry indicated that knockdown of WHSC1 decreased the cell population of cancer cells at the S phase while increasing that at the G(2)/M phase. WHSC1 interacts with some proteins related to the WNT pathway including β-catenin and transcriptionally regulates CCND1, the target gene of the β-catenin/Tcf-4 complex, through histone H3 at lysine 36 trimethylation. This is a novel mechanism for WNT pathway dysregulation in human carcinogenesis, mediated by the epigenetic regulation of histone H3. Because expression levels of WHSC1 are significantly low in most normal tissue types, it should be feasible to develop specific and selective inhibitors targeting the enzyme as antitumor agents that have a minimal risk of adverse reaction.

Indexed as

Wnt Signaling Pathwaybeta CateninCarcinoma, Non-Small-Cell LungCell CycleCell Line, TumorCell ProliferationGene Expression ProfilingGene Expression Regulation, NeoplasticHCT116 CellsHEK293 CellsHep G2 CellsHistone-Lysine N-MethyltransferaseHistonesHumansImmunohistochemistryLung Neoplasmsbeta CateninHistone-Lysine N-MethyltransferaseHistonesNSD2 protein, humanRepressor Proteins

Identifiers

PMID22028615
PMCPMC3201566
OpenAlexW2102769765

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.