Evidence map›Paper›PMID 19706761›Full record

ArticleCancer research2009

A novel splice variant of GLI1 that promotes glioblastoma cell migration and invasion.

Hui-Wen Lo, Hu Zhu, Xinyu Cao, Amy Aldrich, Francis Ali-Osman

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% 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

103 citing papers in PubMed, 1 synthesis or guideline pooled it, 149 citations in OpenAlex.

  1. Pooled it
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43 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

5 authors at 1 institution in 1 country.

Hui-Wen LoDepartment of Surgery, Duke University, Durham, NC 27710, USA. huiwen.lo@duke.edu
Hu Zhu
Xinyu Cao
Amy Aldrich
Francis Ali-Osman
Duke University · US

Funding

Women's Cancer Research ProgramP30CA014236 · NCI · DUKE UNIVERSITY · PI DONNA NIEDZWIECKI · 1985 to 2026
$174.8M
TEMODAR RESISTANCE IN CENTRAL NERVOUS SYSTEMP50CA108786 · NCI · DUKE UNIVERSITY · PI BIGNER, DARELL D · 2004 to 2009
$12.3M
Protein Kinase C and GSTP1 interactions in glioma drug resistanceR01CA127872 · NCI · DUKE UNIVERSITY · PI ALI-OSMAN, FRANCIS · 2008 to 2012
$1.6M
Nuclear EGFR Signaling Network in Human CancerK01CA118423 · NCI · DUKE UNIVERSITY · PI LO, HUI-WEN · 2006 to 2010
$713k
NCI NIH HHS 5P30CA014236-350008NCI NIH HHS K01 CA118423NCI NIH HHS K01-CA118423NCI NIH HHS P50 CA108786NCI NIH HHS P50CA108786NCI NIH HHS R01CA11251NCI NIH HHS R01 CA127872NCI NIH HHS R01CA127872
6 · The paper itself

Abstract

The family of GLI zinc finger transcription factors regulates the expression of genes involved in many important cellular processes, notably embryonal development and cellular differentiation. The glioma-associated oncogene homologue 1 (GLI1) isoform, in particular, has attracted much attention because of its frequent activation in many human cancers and its interactions with other signaling pathways, such as those mediated by K-RAS, transforming growth factor-beta, epidermal growth factor receptor, and protein kinase A. Here, we report the identification of a novel truncated GLI1 splice variant, tGLI1, with an in-frame deletion of 123 bases (41 codons) spanning the entire exon 3 and part of exon 4 of the GLI1 gene. Expression of tGLI1 is undetectable in normal cells but is high in glioblastoma multiforme (GBM) and other cancer cells. Although tGLI1 undergoes nuclear translocalization and transactivates GLI1-binding sites similar to GLI1, unlike GLI1, it is associated with increased motility and invasiveness of GBM cells. Using microarray analysis, we showed >100 genes to be differentially expressed in tGLI1-expressing compared with GLI1-expressing GBM cells, although both cell types expressed equal levels of known GLI1-regulated genes, such as PTCH1. We further showed one of the tGLI1 up-regulated genes, CD24, an invasion-associated gene, to be required for the migratory and invasive phenotype of GBM cells. These data provide conclusive evidence for a novel gain-of-function GLI1 splice variant that promotes migration and invasiveness of GBM cells and open up a new research paradigm on the role of the GLI1 pathway in malignancy.

Indexed as

Alternative SplicingCD24 AntigenCell MovementCodonExonsGene Expression Regulation, NeoplasticGlioblastomaHumansNeoplasm InvasivenessPromoter Regions, GeneticProtein BindingTranscription FactorsZinc Finger Protein GLI1CD24 AntigenCodonGLI1 protein, humanTranscription FactorsZinc Finger Protein GLI1

Identifiers

PMID19706761
PMCPMC2771365
OpenAlexW2164195695

What OpenQuestion holds

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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.