Evidence map›Paper›PMID 17379415›Full record

ArticleBiochimica et biophysica acta2007

Phosphatidylinositol 3-kinase regulation of gastrin-releasing peptide-induced cell cycle progression in neuroblastoma cells.

Titilope A Ishola, JungHee Kang, Jingbo Qiao, B Mark Evers, Dai H Chung

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Peptidergic Systems and Neuroblastoma.International journal of molecular sciences · 2025
    Review
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  9. Differential regulation of cyclin-dependent kinase inhibitors in neuroblastoma cells.Biochemical and biophysical research communications · 2013
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  18. Gastrin-releasing peptide receptor silencing suppresses the tumorigenesis and metastatic potential of neuroblastoma.Proceedings of the National Academy of Sciences of the United States of America · 2008
    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

5 authors at 1 institution in 1 country.

Titilope A IsholaDepartment of Surgery, The University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555, USA.
JungHee Kang
Jingbo Qiao
B Mark Evers
Dai H Chung
The University of Texas Medical Branch at Galveston · US

Funding

TISSUE CULTURE COREP01DK035608 · NIDDK · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI HELLMICH, MARK R · 1986 to 2010
$14.0M
SURGICAL STUDIES OF FUNCTIONAL GENE EXPRESSIONR01DK048498 · NIDDK · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI EVERS, BERNARD MARK · 1996 to 2023
$7.9M
Surgical Studies on the Role on Gastrin-releasing Peptide in NeuroblastomaR01DK061470 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI CHUNG, DAI H. · 2003 to 2018
$4.7M
Surgical Studies of Signaling Pathways in GI CancersR01CA104748 · NCI · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI EVERS, BERNARD MARK · 2004 to 2008
$1.5M
NCI NIH HHS R01 CA104748NIDDK NIH HHS P01 DK035608NIDDK NIH HHS P01 DK35608NIDDK NIH HHS R01 DK048498NIDDK NIH HHS R01 DK061470NIDDK NIH HHS R01 DK48498NIDDK NIH HHS R01 DK61470
6 · The paper itself

Abstract

Gastrin-releasing peptide (GRP), the mammalian equivalent of bombesin (BBS), is an autocrine growth factor for neuroblastoma; its receptor is up-regulated in undifferentiated neuroblastomas. Phosphatidylinositol 3-kinase (PI3K) is a critical cell survival pathway; it is negatively regulated by the PTEN tumor suppressor gene. We have recently found that poorly differentiated neuroblastomas express decreased PTEN protein levels. Moreover, overexpression of the GRP receptor, a member of the G-protein coupled receptor family, down-regulates PTEN expression, resulting in increased neuroblastoma cell growth. Therefore, we sought to determine whether GRP or BBS activates PI3K in neuroblastoma cells (BE(2)-C, LAN-1, SK-N-SH). GRP or BBS treatment rapidly increased phosphorylation of Akt and GSK-3beta in neuroblastoma cells. Inhibition of GRP receptor, with antagonist GRP-H2756 or siRNA, attenuated BBS-induced phosphorylation of Akt. LY294002, a PI3K inhibitor, also abrogated BBS-stimulated phospho-Akt as well as its cell cycle targets. GRP increased G1/S phase progression in SK-N-SH cells. BBS-mediated BrdU incorporation was blocked by LY294002. Our findings identify PI3K as an important signaling pathway for GRP-mediated neuroblastoma cell growth. A novel therapy targeted at GRP/GRP receptor may prove to be an effective treatment option to inhibit PI3K in neuroblastomas.

Indexed as

Autocrine CommunicationG1 PhaseSignal TransductionS PhaseBombesinCell Line, TumorChromonesEnzyme InhibitorsGastrin-Releasing PeptideGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansMorpholinesNeuroblastomaPhosphatidylinositol 3-Kinases2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneBombesinChromonesEnzyme InhibitorsGastrin-Releasing PeptideGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanMorpholinesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanReceptors, BombesinRNA, Small Interfering

Identifiers

PMID17379415
PMCPMC2708969
OpenAlexW2049114878

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.