Evidence map›Paper›PMID 21847707›Full record

ArticleJournal of neuro-oncology2012

The nonsteroidal anti-inflammatory drug celecoxib suppresses the growth and induces apoptosis of human glioblastoma cells via the NF-κB pathway.

Gangadhara Reddy Sareddy, Khamushavalli Geeviman, Chinta Ramulu, Phanithi Prakash Babu

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Article in Journal of neuro-oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
–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

47 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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.

Gangadhara Reddy SareddyDepartment of Biotechnology, School of Life Sciences, University of Hyderabad, Hyderabad 500046, India.
Khamushavalli Geeviman
Chinta Ramulu
Phanithi Prakash Babu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gliomas are devastating primary tumors of the central nervous system and tend to recur even after standard therapy. Celecoxib, the selective COX-2 nonsteroidal anti-inflammatory drug, has anti-neoplastic activity against several malignancies. Accumulating evidence suggests that several COX-2-independent mechanisms may also be involved in the anti-tumor effects of celecoxib. Deregulation of the NF-κB signaling pathway contributes to enhanced glioma cell survival, proliferation, and chemoresistance. In this study, we examined the efficacy of celecoxib in suppressing the growth of glioblastoma cell lines. We observed that treatment with celecoxib significantly reduced the proliferation of a variety of GBM cell lines in a dose-dependent manner and also induced apoptosis, which was evident from enhanced caspase-3 and 8 activity, PARP cleavage, and TUNEL positive cells. Celecoxib treatment significantly down-regulated TNF-α induced NF-κB nuclear translocation, NF-κB DNA binding activity, and NF-κB-dependent reporter gene expression in U373 and T98G cells in a dose-dependent manner. Furthermore, celecoxib suppressed IκBα degradation and phosphorylation and reduced IKK activity in a dose-dependent manner. This study provides evidence that celecoxib suppresses the growth of GBM cell lines partly by inhibiting the NF-κB signaling pathway.

Indexed as

Anti-Inflammatory Agents, Non-SteroidalApoptosisBlotting, WesternBrain NeoplasmsCelecoxibCell Line, TumorCell NucleusCell SurvivalColony-Forming Units AssayColoring AgentsCyclooxygenase 2 InhibitorsCytosolDose-Response Relationship, DrugElectrophoretic Mobility Shift AssayFluorescent Antibody TechniqueGlioblastomaAnti-Inflammatory Agents, Non-SteroidalCelecoxibColoring AgentsCyclooxygenase 2 InhibitorsI-kappa B ProteinsNF-kappa BPyrazolesSulfonamidesTetrazolium SaltsThiazolesthiazolyl blueTumor Necrosis Factor-alpha

Identifiers

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.