Evidence map›Paper›PMID 21677772›Full record

ArticlePloS one2011

Deactivation of signal transducer and activator of transcription 3 reverses chemotherapeutics resistance of leukemia cells via down-regulating P-gp.

Xulong Zhang, Weihua Xiao, Lihua Wang, Zhigang Tian, Jian Zhang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

46 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Natural medicinal compounds target signal transduction pathways to overcome ABC drug efflux transporter-mediated multidrug resistance in cancer.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2023
    Review
  6. Article
  7. High and Low Levels ofInternational journal of molecular sciences · 2023
    Article
  8. Article
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  13. Article
  14. [Mechanism of STAT3 phosphorylation mediated leukemia cells resistance to doxorubicin].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2020
    Article
  15. Article
  16. 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

5 authors at 3 institutions in 1 country.

Xulong ZhangSchool of Pharmaceutical Sciences, Shandong University, Jinan, China.
Weihua Xiao
Lihua Wang
Zhigang Tian
Jian Zhang
Hefei National Center for Physical Sciences at Nanoscale · CNShandong University · CNUniversity of Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multidrug resistance (MDR) caused by overexpression of p-glycoprotein is a major obstacle in chemotherapy of malignant cancer, which usually is characterized by constitutive activation of signal transducer and activator of transcription 3 (STAT3), but their relation between MDR and STAT3 remains unclear. Here, we showed that STAT3 was overexpressed and highly activated in adriamycin-resistant K562/A02 cells compared with its parental K562 cells. Blockade of activation of STAT3 by STAT3 decoy oligodeoxynucleotide (ODN) promoted the accumulation and increased their sensitivity to adriamycin by down-regulating transcription of mdr1 and expression of P-gp, which were further confirmed by using STAT3-specific inhibitor JSI-124. Inhibition of STAT3 could also decrease mdr1 promoter mediated luciferase expression by using mdr1 promoter luciferase reporter construct. Otherwise, activation of STAT3 by STAT3C improved mdr1 transcription and P-gp expression. The ChIP results demonstrated that STAT3 could bind to the potential promoter region of mdr1, and STAT3 decoy depressed the binding. Further mutation assay show +64∼+72 region could be the STAT3 binding site. Our data demonstrate a role of STAT3 in regulation of mdr1 gene expression in myeloid leukemia and suggest that STAT3 may be a promising therapeutic target for overcoming MDR resistance in myeloid leukemia.

Indexed as

Antibiotics, AntineoplasticATP Binding Cassette Transporter, Subfamily B, Member 1Down-RegulationDoxorubicinDrug Resistance, MultipleDrug Resistance, NeoplasmGene Expression Regulation, LeukemicGenes, MDRHumansK562 CellsLeukemiaOligodeoxyribonucleotidesSTAT3 Transcription FactorAntibiotics, AntineoplasticATP Binding Cassette Transporter, Subfamily B, Member 1DoxorubicinOligodeoxyribonucleotidesSTAT3 Transcription Factor

Identifiers

PMID21677772
PMCPMC3108986
OpenAlexW2029505627

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.