Evidence map›Paper›PMID 24755677›Full record

ArticlePloS one2014

NF-kappa B modulation is involved in celastrol induced human multiple myeloma cell apoptosis.

Haiwen Ni, Wanzhou Zhao, Xiangtu Kong, Haitao Li, Jian Ouyang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
16.7field-weighted citation impact, top 1% 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

27 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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  6. Review
  7. Withaferin A and Celastrol Overwhelm Proteostasis.International journal of molecular sciences · 2023
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Mesalazine induces apoptosis via mitochondrial pathway in K562 cell line.Veterinary research forum : an international quarterly journal · 2022
    Article
  13. Article
  14. Review
  15. Article
  16. Article
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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

5 authors at 3 institutions in 1 country.

Haiwen NiAffiliated Hospital of Nanjing University of TCM, Nanjing, China.
Wanzhou ZhaoSino-EU Biomedical Innovation Center (SEBIC), OG Pharma Corporation, Nanjing, China.
Xiangtu KongAffiliated Hospital of Nanjing University of TCM, Nanjing, China.
Haitao LiNanjing University of Chinese Medicine, Nanjing,China.
Jian OuyangDepartment of Hematology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing, China.
Nanjing Traditional Chinese Medicine Hospital · CNNanjing Drum Tower Hospital · CNNanjing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Celastrol is an active compound extracted from the root bark of the traditional Chinese medicine Tripterygium wilfordii Hook F. To investigate the effect of celastrol on human multiple myeloma cell cycle arrest and apoptosis and explore its molecular mechanism of action. The activity of celastrol on LP-1 cell proliferation was detected by WST-8 assay. The celastrol-induced cell cycle arrest was analyzed by flow cytometry after propidium iodide staining. Nuclear translocation of the nuclear factor kappa B (NF-κB) was observed by fluorescence microscope. Celastrol inhibited cell proliferation of LP-1 myeloma cell in a dose-dependent manner with IC50 values of 0.8817 µM, which was mediated through G1 cell cycle arrest and p27 induction. Celastrol induced apoptosis in LP-1 and RPMI 8226 myeloma cells in a time and dose dependent manner, and it involved Caspase-3 activation and NF-κB pathway. Celastrol down-modulated antiapoptotic proteins including Bcl-2 and survivin expression. The expression of NF-κB and IKKa were decreased after celastrol treatment. Celastrol effectively blocked the nuclear translocation of the p65 subunit and induced human multiple myeloma cell cycle arrest and apoptosis by p27 upregulation and NF-kB modulation. It has been demonstrated that the effect of celastrol on NF-kB was HO-1-independent by using zinc protoporphyrin-9 (ZnPPIX), a selective heme oxygenase inhibitor. From the results, it could be inferred that celastrol may be used as a NF-kB inhibitor to inhibit myeloma cell proliferation.

Indexed as

Active Transport, Cell NucleusAntineoplastic AgentsApoptosisCaspase 3Cell Line, TumorCell ProliferationCell SurvivalCyclin-Dependent Kinase Inhibitor p27Drug Screening Assays, AntitumorG1 Phase Cell Cycle CheckpointsHumansI-kappa B ProteinsInhibitory Concentration 50Multiple MyelomaNF-KappaB Inhibitor alphaPentacyclic TriterpenesAntineoplastic AgentsCASP3 protein, humanCaspase 3celastrolCyclin-Dependent Kinase Inhibitor p27I-kappa B ProteinsNF-KappaB Inhibitor alphaNFKBIA protein, humanPentacyclic TriterpenesRELA protein, humanTranscription Factor RelATriterpenes

Identifiers

PMID24755677
PMCPMC3995890
OpenAlexW1969819976

What OpenQuestion holds

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LicenceCC BY
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.