Evidence map›Paper›PMID 21750150›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Homozygously deleted gene DACH1 regulates tumor-initiating activity of glioma cells.

Akira Watanabe, Hideki Ogiwara, Shogo Ehata, Akitake Mukasa, Shumpei Ishikawa, Daichi Maeda, Keisuke Ueki, Yasushi Ino, Tomoki Todo, Yasuhiro Yamada and 4 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 42 citations in OpenAlex.

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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

14 authors at 5 institutions in 2 countries.

Akira WatanabeResearch Center for Advanced Science and Technology, University of Tokyo, Tokyo, Japan.
Hideki Ogiwara
Shogo Ehata
Akitake Mukasa
Shumpei Ishikawa
Daichi Maeda
Keisuke Ueki
Yasushi Ino
Tomoki Todo
Yasuhiro Yamada
Masashi Fukayama
Nobuhito Saito
Kohei Miyazono
Hiroyuki Aburatani
Neurology, Inc · USThe University of Tokyo · JPKyoto University · JPDokkyo Medical University · JPJapan Science and Technology Agency · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss or reduction in function of tumor suppressor genes contributes to tumorigenesis. Here, by allelic DNA copy number analysis using single-nucleotide polymorphism genotyping array and mass spectrometry, we report homozygous deletion in glioblastoma multiformes at chromosome 13q21, where DACH1 gene is located. We found decreased cell proliferation of a series of glioma cell lines by forced expression of DACH1. We then generated U87TR-Da glioma cells, where DACH1 expression could be activated by exposure of the cells to doxycycline. Both ex vivo cellular proliferation and in vivo growth of s.c. transplanted tumors in mice are reduced in U87TR-Da cells with DACH1 expression (U87-DACH1-high), compared with DACH1-nonexpressing U87TR-Da cells (U87-DACH1-low). U87-DACH1-low cells form spheroids with CD133 and Nestin expression in serum-free medium but U87-DACH1-high cells do not. Compared with spheroid-forming U87-DACH1-low cells, adherent U87-DACH1-high cells display lower tumorigenicity, indicating DACH1 decreases the number of tumor-initiating cells. Gene expression analysis and chromatin immunoprecipitation assay reveal that fibroblast growth factor 2 (FGF2/bFGF) is transcriptionally repressed by DACH1, especially in cells cultured in serum-free medium. Exogenous bFGF rescues spheroid-forming activity and tumorigenicity of the U87-DACH1-high cells, suggesting that loss of DACH1 increases the number of tumor-initiating cells through transcriptional activation of bFGF. These results illustrate that DACH1 is a distinctive tumor suppressor, which does not only suppress growth of tumor cells but also regulates bFGF-mediated tumor-initiating activity of glioma cells.

Indexed as

AllelesAnimalsBrain NeoplasmsCell Line, TumorCell ProliferationChromosomes, Human, Pair 13DoxycyclineEye ProteinsFibroblast Growth Factor 2Gene DeletionGene DosageGene ExpressionGenes, Tumor SuppressorGlioblastomaGliomaHomozygoteDACH1 protein, humanDoxycyclineEye ProteinsFibroblast Growth Factor 2Transcription Factors

Identifiers

PMID21750150
PMCPMC3145721
OpenAlexW2090805312

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.