Evidence map›Paper›PMID 22833150›Full record

ArticleJournal of cancer research and clinical oncology2012

Growth inhibitory effect of dihydroartemisinin on Bcr/Abl+ chronic myeloid leukemia K562 cells involve AKT, ERK and NF-κB modulation.

Jun Lee, Guobing Zhang, Xiuhua Wu, Feilong Xu, Jun Zhou, Xingguo Zhang

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  6. Article
  7. Antitumor Research on Artemisinin and Its Bioactive Derivatives.Natural products and bioprospecting · 2018
    Review
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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

6 authors at 1 institution in 1 country.

Jun LeeDepartment of Clinical Pharmacology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China. junleepost@hotmail.com
Guobing Zhang
Xiuhua Wu
Feilong Xu
Jun Zhou
Xingguo Zhang
Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeIn our previous publication, we have shown that dihydroartemisinin could significantly inhibit the growth of CML K562 cells by its anti-proliferative and inducing apoptotic effects. Given the pivotal effect of Bcr/Abl tyrosine kinase and its downstream signal factors on CML cell proliferation and survival, we extend our study to investigate the effect of DHA on Bcr/Abl and related signal factors to further illuminate the possible mechanisms of the effect of DHA on CML cells.

methodsThe expression of Bcr/Abl was analyzed with PCR and Western blotting methods at both mRNA and protein levels. Measurement of protein expression and tyrosine phosphorylation activity of Bcr/Abl, AKT, ERK1/2, NF-κB and cytochrome c were performed with Western blotting and immunoprecipitation methods. Using the activity kits analyzed the activity of caspase 9 and caspase 3.

resultsThe treatment with DHA results in a significant suppression on Bcr/Abl expression and leads to a concentration-dependent reduction on the Bcr/Abl tyrosine activity. Moreover, it also results in a strong influence on the downstream signal factors of Bcr/Abl, which includes inhibition of tyrosine kinase activity of AKT and ERK1/2, suppression of NF-κB protein expression, promotion of the cytochrome c release and the consequential activation of caspase 3/9 in CML K562 cells.

conclusionsTogether with our previous report, our data show that the growth inhibitory effect of DHA on CML cells might be due to the influence on Bcr/Abl expression and its downstream signal factors. DHA might be a potential novel anti-CML drug candidate and worthy of further study.

Indexed as

ArtemisininsCaspase 3Caspase 9Cell Line, TumorCell ProliferationCytochromes cDown-RegulationFusion Proteins, bcr-ablGrowth InhibitorsHumansK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMAP Kinase Signaling SystemNF-kappa BPhosphorylationProtein-Tyrosine KinasesArtemisininsartenimolCaspase 3Caspase 9Cytochromes cFusion Proteins, bcr-ablGrowth InhibitorsNF-kappa BProtein-Tyrosine KinasesProto-Oncogene Proteins c-aktRNA, Messenger

Identifiers

PMID22833150
PMCPMC11824778
OpenAlexW2024050143

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.