Evidence map›Paper›PMID 24893952›Full record

ArticleBMC cancer2014

Lipid metabolism enzyme ACSVL3 supports glioblastoma stem cell maintenance and tumorigenicity.

Peng Sun, Shuli Xia, Bachchu Lal, Xiaohai Shi, Kil Sung Yang, Paul A Watkins, John Laterra

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

35 citing papers in PubMed, 52 citations in OpenAlex.

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  7. Glioblastoma Metabolism: Insights and Therapeutic Strategies.International journal of molecular sciences · 2023
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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

7 authors at 4 institutions in 1 country.

Peng Sun
Shuli Xia
Bachchu Lal
Xiaohai Shi
Kil Sung Yang
Paul A Watkins
John LaterraHugo W, Moser Research Institute at Kennedy Krieger, Baltimore, MD, USA. laterra@kennedykrieger.org.
Kennedy Krieger Institute · USJohns Hopkins Medicine · USJohns Hopkins University · USThe University of Texas MD Anderson Cancer Center · US

Funding

Mechanisms of Chemo/Radioresistance in Human GliomasR01NS043987 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI LATERRA, JOHN J, ROSEN, ELIOT M. · 2003 to 2012
$4.9M
Brain Cancer Stem Cell Reprogramming by c-MetR01NS073611 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI LATERRA, JOHN J · 2012 to 2016
$1.8M
Acyl-CoA synthetase ACSVL3 in Malignant Glioma: Metabolism and Oncogenic CellularR01NS062043 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI WATKINS, PAUL A. · 2009 to 2013
$1.7M
NINDS NIH HHS NS062043NINDS NIH HHS NS073611NINDS NIH HHS NS43987
6 · The paper itself

Abstract

backgroundTargeting cell metabolism offers promising opportunities for the development of drugs to treat cancer. We previously found that the fatty acyl-CoA synthetase VL3 (ACSVL3) is elevated in malignant brain tumor tissues and involved in tumorigenesis. This study investigates the role of ACSVL3 in the maintenance of glioblastoma multiforme (GBM) stem cell self-renewal and the capacity of GBM stem cells to initiate tumor xenograft formation.

methodsWe examined ACSVL3 expression during differentiation of several GBM stem cell enriched neurosphere cultures. To study the function of ACSVL3, we performed loss-of-function by using small interfering RNAs to target ACSVL3 and examined stem cell marker expression, neurosphere formation and tumor initiation properties.

resultsACSVL3 expression levels were substantially increased in GBM stem cell enriched neurosphere cultures and decreased after differentiation of the neurospheres. Down-regulating ACSVL3 with small inhibiting RNAs decreased the expression of markers and regulators associated with stem cell self-renewal, including CD133, ALDH, Musashi-1 and Sox-2. ACSVL3 knockdown in neurosphere cells led to increased expression of differentiation markers GFAP and Tuj1. Furthermore, ACSVL3 knockdown reduced anchorage-independent neurosphere cell growth, neurosphere-forming capacity as well as self-renewal of these GBM stem cell enriched neurosphere cultures. In vivo studies revealed that ACSVL3 loss-of-function substantially inhibited the ability of neurosphere cells to propagate orthotopic tumor xenografts. A link between ACSVL3 and cancer stem cell phenotype was further established by the findings that ACSVL3 expression was regulated by receptor tyrosine kinase pathways that support GBM stem cell self-renewal and tumor initiation, including EGFR and HGF/c-Met pathways.

conclusionsOur findings indicate that the lipid metabolism enzyme ACSVL3 is involved in GBM stem cell maintenance and the tumor-initiating capacity of GBM stem cell enriched-neurospheres in animals.

Indexed as

AnimalsBrain NeoplasmsCarcinogenesisCell DifferentiationCell Line, TumorCoenzyme A LigasesGene Expression Regulation, NeoplasticGlioblastomaHumansLipid MetabolismLong-Chain-Fatty-Acid-CoA LigaseMiceNeoplastic Stem CellsSignal TransductionXenograft Model Antitumor AssaysCoenzyme A LigasesLong-Chain-Fatty-Acid-CoA Ligase

Identifiers

PMID24893952
PMCPMC4055398
OpenAlexW2170731941

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.