Evidence map›Paper›PMID 26666667›Full record

ArticleMolecular neurobiology2016

Ibuprofen Induces Mitochondrial-Mediated Apoptosis Through Proteasomal Dysfunction.

Arun Upadhyay, Ayeman Amanullah, Deepak Chhangani, Vibhuti Joshi, Ribhav Mishra, Amit Mishra

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Cimetidine and Ibuprofen Modulate T Cell Responses in a Mouse Model of Breast Cancer.Asian Pacific journal of cancer prevention : APJCP · 2022
    Article
  8. Anti-Inflammatory Potentials of the n-Hexane Fraction ofJournal of inflammation research · 2021
    Article
  9. Article
  10. Article
  11. 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

6 authors at 1 institution in 1 country.

Arun UpadhyayCellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Rajasthan, India, 342011.
Ayeman AmanullahCellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Rajasthan, India, 342011.
Deepak ChhanganiCellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Rajasthan, India, 342011.
Vibhuti JoshiCellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Rajasthan, India, 342011.
Ribhav MishraCellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Rajasthan, India, 342011.
Amit MishraCellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Rajasthan, India, 342011. amit@iitj.ac.in.
Indian Institute of Technology Jodhpur · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In routine course of life, nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed antipyretic, analgesic, and anti-inflammatory drugs. It is a well-proposed notion that treatment of NSAIDs may induce anti-proliferative effects in numerous cancer cells. Ibuprofen from isobutylphenylpropanoic acid is NSAID and used to relieve fever, pain, and inflammation. It is also used for juvenile idiopathic arthritis, rheumatoid arthritis, patent ductus arteriosus, and for pericarditis. Despite few emerging studies have expanded the fundamental concept that the treatment of NSAIDs influences apoptosis in cancer cells, however the NSAID-mediated precise mechanisms that determine apoptosis induction without producing adverse consequences in variety of cancer cells are largely unknown. In our present study, we have observed that ibuprofen reduces proteasome activity, enhances the aggregation of ubiquitylated abnormal proteins, and also elevates the accumulation of crucial proteasome substrates. Ibuprofen treatment causes mitochondrial abnormalities and releases cytochrome c into cytosol. Perhaps, the more detailed study is needed in the future to elucidate the molecular mechanisms of NSAIDs that can induce apoptosis without adverse effects and produce effective anti-tumor effects and consequently help in neurodegeneration and ageing.

Indexed as

A549 CellsAnimalsApoptosisCell NucleusCell Nucleus ShapeCell ShapeChlorocebus aethiopsChromatinCOS CellsCytochromes cDNA FragmentationHumansIbuprofenInclusion BodiesMembrane Potential, MitochondrialMitochondriaChromatinCytochromes cIbuprofenNF-KappaB Inhibitor alphaProteasome Endopeptidase ComplexProtein AggregatesUbiquitinated ProteinsAgeingApoptosisIbuprofenMitochondrial dysfunctionNeurodegenerationNSAIDsProteasome

Identifiers

PMID26666667
OpenAlexW2294686368

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.