Evidence map›Paper›PMID 17335970›Full record

ArticleNeuroscience letters2007

5-Aminolevulinic acid-based photodynamic therapy suppressed survival factors and activated proteases for apoptosis in human glioblastoma U87MG cells.

Surajit Karmakar, Naren L Banik, Sunil J Patel, Swapan K Ray

Abstract read
In one paragraph

Article in Neuroscience letters, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
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

28 citing papers in PubMed.

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  14. Photodynamic therapy mediated by 5-aminolevulinic acid suppresses gliomas growth by decreasing the microvessels.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2015
    Article
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  16. Sodium butyrate increases the effect of the photodynamic therapy: a mechanism that involves modulation of gene expression and differentiation in astrocytoma cells.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2012
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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

4 authors.

Surajit KarmakarDepartment of Neurosciences, Medical University of South Carolina, 96 Jonathan Lucas Street, Suite 323K, Charleston, SC 29425, USA.
Naren L Banik
Sunil J Patel
Swapan K Ray

Funding

DIFFERENTIATION AND APOPTOSIS IN MALIGNANT NEUROBLASTOMAR01NS057811 · NINDS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI RAY, SWAPAN K. · 2006 to 2009
$1.3M
PROTEOLYTIC CONTROL OF GLIOBLASTOMAR01CA091460 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI RAY, SWAPAN K · 2003 to 2007
$1.1M
NCI NIH HHS R01 CA091460NCI NIH HHS R01 CA091460-04NCI NIH HHS R01 CA 91460NINDS NIH HHS R01 NS057811NINDS NIH HHS R01 NS057811-01A1NINDS NIH HHS R01 NS 57811
6 · The paper itself

Abstract

Glioblastoma is the most common astrocytic brain tumor in humans. Current therapies for this malignancy are mostly ineffective. Photodynamic therapy (PDT), an exciting treatment strategy based on activation of a photosensitizer, has not yet been extensively explored for treating glioblastoma. We used 5-aminolevulinic acid (5-ALA) as a photosensitizer for PDT to induce apoptosis in human malignant glioblastoma U87MG cells and to understand the underlying molecular mechanisms. Trypan blue dye exclusion test showed a decrease in cell viability after exposure to increasing doses of 5-ALA for 4h followed by PDT with a broad spectrum blue light (400-550 nm) at a dose of 18J/cm(2) for 1h and then incubation at 37 degrees C for 4h. Following 0.5 and 1mM 5-ALA-based PDT (5-ALA-PDT), Wright staining and ApopTag assay showed occurrence of apoptosis morphologically and biochemically, respectively. After 5-ALA-PDT, down regulation of nuclear factor kappa B (NFkappaB) and baculovirus inhibitor-of-apoptosis repeat containing-3 (BIRC-3) protein indicated inhibition of survival signals. Besides, 5-ALA-PDT caused increase in Bax:Bcl-2 ratio and mitochondrial release of cytochrome c and apoptosis-inducing factor (AIF). Activation of calpain, caspase-9, and caspase-3 occurred in course of apoptosis. Calpain and caspase-3 activities cleaved alpha-spectrin at specific sites generating 145kD spectrin breakdown product (SBDP) and 120kD SBDP, respectively. The results suggested that 5-ALA-PDT induced apoptosis in U87MG cells by suppression of survival signals and activation of proteolytic pathways. Thus, 5-ALA-PDT can be an effective strategy for inducing apoptosis in glioblastoma.

Indexed as

Aminolevulinic AcidApoptosisApoptosis Inducing FactorApoptosis Regulatory ProteinsBaculoviral IAP Repeat-Containing 3 ProteinBrain NeoplasmsCalpainCaspasesCell Line, TumorCell SurvivalDose-Response Relationship, DrugGlioblastomaHumansInhibitor of Apoptosis ProteinsNF-kappa BPeptide HydrolasesAminolevulinic AcidApoptosis Inducing FactorApoptosis Regulatory ProteinsBaculoviral IAP Repeat-Containing 3 ProteinBIRC3 protein, humanCalpainCaspasesInhibitor of Apoptosis ProteinsNF-kappa BPeptide HydrolasesUbiquitin-Protein Ligases

Identifiers

PMID17335970
PMCPMC2533742

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.