Evidence map›Paper›PMID 25628518›Full record

ArticleProteome science2015

Comparative proteomics analysis of differential proteins in respond to doxorubicin resistance in myelogenous leukemia cell lines.

Shi Qinghong, Gao Shen, Song Lina, Zhao Yueming, Li Xiaoou, Wu Jianlin, He Chengyan, Li Hongjun, Zhao Haifeng

Open access · goldAbstract read
In one paragraph

Article in Proteome science, 2015. 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
4.7field-weighted citation impact, top 4% 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, 58 citations in OpenAlex.

  1. Doxorubicin-Induced Cardiotoxicity: A Comprehensive Update.Journal of cardiovascular development and disease · 2025
    Review
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  6. Sorcin: a novel potential target in therapies of cancers.Cancer management and research · 2019
    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

9 authors at 5 institutions in 2 countries.

Shi QinghongJilin University China-Japan Union Hospital, Changchun, 130033 China.
Gao ShenJilin University China-Japan Union Hospital, Changchun, 130033 China.
Song LinaJilin University China-Japan Union Hospital, Changchun, 130033 China.
Zhao YuemingJilin University China-Japan Union Hospital, Changchun, 130033 China ; Tumor Hospital of Jilin Province, Changchun, 130021 China.
Li XiaoouTumor Hospital of Jilin Province, Changchun, 130021 China.
Wu JianlinState Key Laboratory for Quality Research in Chinese Medicines, Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau, China.
He ChengyanJilin University China-Japan Union Hospital, Changchun, 130033 China.
Li HongjunJilin University China-Japan Union Hospital, Changchun, 130033 China.
Zhao HaifengJiamusi University, Jiamusi, 154002 China.
Jilin University · CNUnion Hospital · CNJiamusi University · CNJilin Province Tumor Hospital · CNMacau University of Science and Technology · MO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChemoresistance remains a significant challenge in chronic myelogenous leukemia (CML) management, which is one of the most critical prognostic factors. Elucidation the molecular mechanisms underlying the resistance to chemoresistance may lead to better clinical outcomes.

resultsIn order to identify potential protein targets involved in the drug-resistant phenotype of leukemia, especially the chronic myelogenous leukemia (CML), we used a high-resolution "ultra-zoom" 2DE-based proteomics approach to characterize global protein expression patterns in doxorubicin-resistant myelogenous leukemia cells compared with parental control cells. Ultra-high resolution of 2DE was achieved by using a series of slightly overlapping narrow-range IPG strips during isoelectric focusing (IEF) separation. A total number of 44 proteins with altered abundances were detected and identified by MALDI-TOF or LC-MS/MS. Among these proteins, enolase, aldolase, HSP70 and sorcin were up-regulated in doxorubicin-resistant myelogenous leukemia cell line, whereas HSP27 was down-regulated. Some of the results have been validated by Western blotting. Both enolase and aldolase were first reported to be involved in chemoresistance, suggesting that process of glycolysis in doxorubicin-resistant myelogenous leukemia cells was accelerated to some extent to provide more energy to survive chemical stress. Possible roles of most of the identified proteins in development of chemoresistance in myelogenous leukemia cells were fully discussed. The results presented here could provide clues to further study for elucidating the mechanisms underlying drug resistance in leukemia.

conclusionsAs a whole, under the chemical stress, the doxorubicin-resistant myelogenous leukemia cells may employ various protective strategies to survive. These include: (i) pumping the cytotoxic drug out of the cells by P-glycoprotein, (ii) increased storage of fermentable fuel, (iii) sophisticated cellular protection by molecular chaperones, (iv) improved handling of intracellular calcium, (v) increased glucose utilization via increased rates of glycolysis. In the present study, proteomic analysis of leukemia cells and their drug resistant variants revealed multiple alterations in protein expression. Our results indicate that the development of drug resistance in doxorubicin-resistant myelogenous leukemia cells is a complex phenomenon undergoing several mechanisms.

Identifiers

PMID25628518
PMCPMC4307195
OpenAlexW2126497158

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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.