Evidence map›Paper›PMID 19894226›Full record

ArticleCancer2010

Flavonoids activated caspases for apoptosis in human glioblastoma T98G and U87MG cells but not in human normal astrocytes.

Arabinda Das, Naren L Banik, Swapan K Ray

Open access · bronzeAbstract read
In one paragraph

Article in Cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
7.1field-weighted citation impact, top 3% 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

93 citing papers in PubMed, 203 citations in OpenAlex.

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  20. Downregulation ofIranian journal of pharmaceutical research : IJPR · 2022
    Article

33 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

3 authors at 2 institutions in 1 country.

Arabinda DasDepartment of Neurosciences, Medical University of South Carolina, Charleston, SC 29209, USA. swapan.ray@uscmed.sc.edu
Naren L Banik
Swapan K Ray
Medical University of South Carolina · USUniversity of South Carolina · US

Funding

Extra-nigral Neurodegeneration in Experimental Parkinson's DiseaseR01NS062327 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BANIK, NAREN L · 2009 to 2013
$1.6M
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 CA091460NINDS NIH HHS R01 NS057811NINDS NIH HHS R01 NS062327
6 · The paper itself

Abstract

backgroundHuman glioblastoma is a deadly brain cancer that continues to defy all current therapeutic strategies. The authors induced apoptosis in human glioblastoma T98G and U87MG cells after treatment with apigenin, (-)-epigallocatechin, (-)-epigallocatechin-3-gallate (EGCG), and genistein, which did not induce apoptosis in human normal astrocytes.

methodsInduction of apoptosis was examined using Wright staining and ApopTag assay. Production of reactive oxygen species (ROS) and increase in intracellular free Ca(2+) were measured by fluorescent probes. Analysis of mRNA and Western blotting indicated increases in expression and activities of the stress kinases and cysteine proteases for apoptosis. JC-1 showed changes in mitochondrial membrane potential (DeltaPsi(m)), and use of specific inhibitors confirmed activation of kinases and proteases in apoptosis.

resultsTreatment of glioblastoma cells with apigenin, (-)-epigallocatechin, EGCG, or genistein triggered ROS production that induced apoptosis with phosphorylation of p38 mitogen-activated protein kinase (MAPK) and activation of the redox-sensitive c-Jun N-terminal kinase 1 pathway. Pretreatment of cells with ascorbic acid attenuated ROS production and p38 MAPK phosphorylation. Increases in intracellular free Ca2+ and activation of caspase-4 indicated involvement of endoplasmic reticulum stress in apoptosis. Other events in apoptosis included overexpression of Bax, loss of DeltaPsi(m), mitochondrial release of cytochrome c and Smac into the cytosol, down-regulation of baculoviral inhibitor-of-apoptosis repeat-containing proteins, and activation of calpain, caspase-9, and caspase-3. (-)-Epigallocatechin and EGCG also induced caspase-8 activity. Apigenin, (-)-epigallocatechin, EGCG, and genistein did not induce apoptosis in human normal astrocytes.

conclusionsResults strongly suggest that flavonoids are potential therapeutic agents for induction of apoptosis in human glioblastoma cells.

Indexed as

ApoptosisAstrocytesBH3 Interacting Domain Death Agonist ProteinBrain NeoplasmsCaspase 8CaspasesCatechinCell LineCell Line, TumorEnzyme ActivationFlavonoidsGlioblastomaHumansMembrane Potential, MitochondrialMitogen-Activated Protein Kinase 8Reactive Oxygen SpeciesBH3 Interacting Domain Death Agonist ProteinCaspase 8CaspasesCatechinepigallocatechin gallateFlavonoidsgallocatecholMitogen-Activated Protein Kinase 8Reactive Oxygen Species

Identifiers

PMID19894226
PMCPMC3159962
OpenAlexW1996149494

What OpenQuestion holds

Textmetadata
LicenceTDM
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.