Evidence map›Paper›PMID 23018344›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2012

Inhibition of p38 MAPK diminishes doxorubicin-induced drug resistance associated with P-glycoprotein in human leukemia K562 cells.

Yinghui Chen, Yongbo Zhao, Cuicui Wang, Xia Xiao, Xiaoyong Zhou, Guoxiong Xu

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 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
1.2field-weighted citation impact, top 21% 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, 26 citations in OpenAlex.

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  12. MDR1 polymorphisms and idiopathic nephrotic syndrome in Slovak children: preliminary results.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Article
  13. Activity of sputum p38 MAPK is correlated with airway inflammation and reduced FEV1 in COPD patients.Medical science monitor : international medical journal of experimental and clinical research · 2013
    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 2 institutions in 1 country.

Yinghui ChenDepartment of Neurology, Jinshan Hospital, Fudan University, Shanghai, PR China. cyh1973131@163.com
Yongbo Zhao
Cuicui Wang
Xia Xiao
Xiaoyong Zhou
Guoxiong Xu
Jinshan Hospital of Fudan University · CNShanghai East Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSeveral studies have shown that multidrug transporters, such as P-glycoprotein (PGP), are involved in cell resistance to chemotherapy and refractory epilepsy. The p38 mitogen-activated protein kinase (MAPK) signaling pathway may increase PGP activity. However, p38-mediated drug resistance associated with PGP is unclear. Here, we investigated p38-mediated doxorubicin-induced drug resistance in human leukemia K562 cells. MATERIAL/

methodsThe expression of PGP was detected by RT-PCR, Western blot, and immunocytochemistry. Cell viability and half-inhibitory concentrations (IC50) were determined by CCK-8 assay. The intracellular concentration of drugs was measured by HPLC.

resultsA doxorubicin-induced PGP overexpression cell line, K562/Dox, was generated. The p38 inhibitor SB202190 significantly decreased MDR1 mRNA expression, as well as PGP, in K562/Dox cells. The IC50 of phenytoin sodium and doxorubicin in K562/Dox cells was significantly higher than that in wild-type K562 cells, indicating the drug resistance of K562/Dox cells. During the blocking of p38 activity in the presence of SB202190, cell number was significantly reduced after the phenytoin sodium and doxorubicin treatment, and the IC50 of phenytoin sodium and doxorubicin was decreased in K562/Dox cells. HPLC showed that the intracellular levels of phenytoin sodium and doxorubicin were significantly lower in K562/Dox cells than those in K562 cells. The decrease of the intracellular level of these drugs was significantly abolished in the presence of SB202190.

conclusionsOur study demonstrated that p38 is, at least in part, involved in doxorubicin-induced drug resistance. The mechanistic study of MAPK-mediated PGP and the action of SB202190 need further investigation.

Indexed as

ATP Binding Cassette Transporter, Subfamily B, Member 1Cell SurvivalDose-Response Relationship, DrugDoxorubicinDrug Resistance, NeoplasmHumansImidazolesK562 CellsLeukemiap38 Mitogen-Activated Protein KinasesPhenytoinProtein Kinase InhibitorsPyridines4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazoleATP Binding Cassette Transporter, Subfamily B, Member 1DoxorubicinImidazolesp38 Mitogen-Activated Protein KinasesPhenytoinProtein Kinase InhibitorsPyridines

Identifiers

PMID23018344
PMCPMC3560559
OpenAlexW2019386839

What OpenQuestion holds

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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.