Evidence map›Paper›PMID 30909944›Full record

ArticleBMC complementary and alternative medicine2019

Deciphering the mechanism of Indirubin and its derivatives in the inhibition of Imatinib resistance using a "drug target prediction-gene microarray analysis-protein network construction" strategy.

Huayao Li, Lijuan Liu, Jing Zhuang, Cun Liu, Chao Zhou, Jing Yang, Chundi Gao, Gongxi Liu, Changgang Sun

Open access · goldAbstract read
In one paragraph

Article in BMC complementary and alternative medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

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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

9 authors at 3 institutions in 1 country.

Huayao LiFirst Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan, 250014, Shandong, People's Republic of China.
Lijuan LiuFirst Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan, 250014, Shandong, People's Republic of China.
Jing ZhuangDepartment of Oncology, Affilited Hospital of Weifang Medical University, Weifang, 261031, Shandong, People's Republic of China.
Cun LiuFirst Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan, 250014, Shandong, People's Republic of China.
Chao ZhouDepartmen of Oncology, Weifang Traditional Chinese Hospital, Weifang, 261041, Shandong, People's Republic of China.
Jing YangDepartmen of Oncology, Weifang Traditional Chinese Hospital, Weifang, 261041, Shandong, People's Republic of China.
Chundi GaoFirst Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan, 250014, Shandong, People's Republic of China.
Gongxi LiuDepartmen of Oncology, Weifang Traditional Chinese Hospital, Weifang, 261041, Shandong, People's Republic of China.
Changgang SunDepartment of Oncology, Affilited Hospital of Weifang Medical University, Weifang, 261031, Shandong, People's Republic of China. scgdoctor@126.com.ORCID http://orcid.org/0000-0002-6648-3602
Shandong University of Traditional Chinese Medicine · CNWeifang Chinese Medicine Hospital · CNWeifang Medical University · CN

Funding

National Natural Science Foundation of China (CN) 81673799National Natural Science Foundation of China Youth Fund 81703915
6 · The paper itself

Abstract

backgroundThe introduction of imatinib revolutionized the treatment of chronic myeloid leukaemia (CML), substantially extending patient survival. However, imatinib resistance is currently a clinical problem for CML. It is very importantto find a strategy to inhibit imatinib resistance.

methods(1) We Identified indirubin and its derivatives and predicted its putative targets; (2) We downloaded data of the gene chip GSE2810 from the Gene Expression Omnibus (GEO) database and performed GEO2R analysis to obtain differentially expressed genes (DEGs); and (3) we constructed a P-P network of putative targets and DEGs to explore the mechanisms of action and to verify the results of molecular docking.

resultWe Identified a total of 42 small-molecule compounds, of which 15 affected 11 putative targets, indicating the potential to inhibit imatinib resistance; the results of molecular docking verified these results. Six biomarkers of imatinib resistance were characterised by analysing DEGs.

conclusionThe 15 small molecule compounds inhibited imatinib resistance through the cytokine-cytokine receptor signalling pathway, the JAK-stat pathway, and the NF-KB signalling pathway. Indirubin and its derivatives may be new drugsthat can combat imatinib resistance.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsCell Line, TumorDatabases, FactualDown-RegulationDrug Delivery SystemsHumansImatinib MesylateIndolesMolecular Dynamics SimulationOligonucleotide Array Sequence AnalysisProtein Interaction MappingAntineoplastic AgentsImatinib MesylateindirubinIndolesDerivativesDrug target predictionGene microarray analysisImatinib resistanceIndirubinProtein network construction

Identifiers

PMID30909944
PMCPMC6434895
OpenAlexW2937356408

What OpenQuestion holds

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LicenceCC BY
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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.