Evidence map›Paper›PMID 18322795›Full record

ArticleNeurochemical research2008

Underlying mechanism of quercetin-induced cell death in human glioma cells.

Eui Joong Kim, Chang Hwa Choi, Ji Yeon Park, Soo Kyung Kang, Yong Keun Kim

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 83 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Heat Shock Proteins in Glioblastoma Biology: Where Do We Stand?International journal of molecular sciences · 2019
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Inhibition of autophagy induced by quercetin at a late stage enhances cytotoxic effects on glioma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  18. Review
  19. Article
  20. Review
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.

Eui Joong KimDepartment of Neurosurgery, College of Medicine, Pusan National University, Pusan 602-739, South Korea.
Chang Hwa Choi
Ji Yeon Park
Soo Kyung Kang
Yong Keun Kim
Pusan National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There has been considerable interest in recent years in the anti-tumor activities of flavonoids. Quercetin, a ubiquitous bioactive flavonoid, can inhibit proliferation and induce apoptosis in a variety of cancer cells. However, the precise molecular mechanism by which quercetin induces apoptosis in cancer cells is poorly understood. The present study was undertaken to examine the effect of quercetin on cell viability and to determine its underlying mechanism in human glioma cells. Quercetin resulted in loss of cell viability in a dose- and time-dependent manner and the decrease in cell viability was mainly attributed to cell death. Quercetin did not increase reactive oxygen species (ROS) generation and the quercetin-induced cell death was also not affected by antioxidants, suggesting that ROS generation is not involved in loss of cell viability. Western blot analysis showed that quercetin treatment caused rapid reduction in phosphorylation of extracellular signal-regulated kinase (ERK) and Akt. Transient transfection with constitutively active forms of MEK and Akt protected against the quercetin-induced loss of cell viability. Quercetin-induced depolarization of mitochondrial membrane potential. Caspase activity was stimulated by quercetin and caspase inhibitors prevented the quercetin-induced loss of cell viability. Quercetin resulted in a decrease in expression of survivin, antiapoptotic proteins. Taken together, these findings suggest that quercetin results in human glioma cell death through caspase-dependent mechanisms involving down-regulation of ERK, Akt, and survivin.

Indexed as

AnimalsAntioxidantsCaspasesCell DeathCell Line, TumorCell SurvivalEnzyme ActivationExtracellular Signal-Regulated MAP KinasesGliomaHumansInhibitor of Apoptosis ProteinsMicrotubule-Associated ProteinsMitochondriaNeoplasm ProteinsProto-Oncogene Proteins c-aktQuercetinAntioxidantsBIRC5 protein, humanCaspasesExtracellular Signal-Regulated MAP KinasesInhibitor of Apoptosis ProteinsMicrotubule-Associated ProteinsNeoplasm ProteinsProto-Oncogene Proteins c-aktQuercetinReactive Oxygen SpeciesSurvivinX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID18322795
OpenAlexW2045159353

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.