Evidence map›Paper›PMID 25193854›Full record

ArticleOncotarget2014

Anti-rheumatic agent auranofin induced apoptosis in chronic myeloid leukemia cells resistant to imatinib through both Bcr/Abl-dependent and -independent mechanisms.

Xin Chen, Xianping Shi, Chong Zhao, Xiaofen Li, Xiaoying Lan, Shouting Liu, Hongbiao Huang, Ningning Liu, Siyan Liao, Dan Zang and 6 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

44 citing papers in PubMed, 80 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

16 authors at 5 institutions in 2 countries.

Xin ChenState Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Departments of Pathophysiology and Biochemistry, Guangzhou Medical University, Guangdong 510182, China; These Authors contributed equally to this work.
Xianping ShiState Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Departments of Pathophysiology and Biochemistry, Guangzhou Medical University, Guangdong 510182, China; These Authors contributed equally to this work.
Chong ZhaoState Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Departments of Pathophysiology and Biochemistry, Guangzhou Medical University, Guangdong 510182, China; These Authors contributed equally to this work.
Xiaofen LiState Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Departments of Pathophysiology and Biochemistry, Guangzhou Medical University, Guangdong 510182, China.
Xiaoying LanState Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Departments of Pathophysiology and Biochemistry, Guangzhou Medical University, Guangdong 510182, China.
Shouting LiuState Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Departments of Pathophysiology and Biochemistry, Guangzhou Medical University, Guangdong 510182, China.
Hongbiao HuangState Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Departments of Pathophysiology and Biochemistry, Guangzhou Medical University, Guangdong 510182, China.
Ningning LiuState Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Departments of Pathophysiology and Biochemistry, Guangzhou Medical University, Guangdong 510182, China; Guangzhou Research Institute of Cardiovascular Disease, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510260, People's Republic of China.
Siyan LiaoState Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Departments of Pathophysiology and Biochemistry, Guangzhou Medical University, Guangdong 510182, China.
Dan ZangState Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Departments of Pathophysiology and Biochemistry, Guangzhou Medical University, Guangdong 510182, China.
Wenbin SongState Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Departments of Pathophysiology and Biochemistry, Guangzhou Medical University, Guangdong 510182, China.
Quentin LiuSun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou 510060, China.
Bing Z CarterSection of Molecular Hematology and Therapy, Department of leukemia, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA.
Q Ping DouState Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Departments of Pathophysiology and Biochemistry, Guangzhou Medical University, Guangdong 510182, China; The Molecular Therapeutics Program, Barbara Ann Karmanos Cancer Institute, and Departments of Oncology, Pharmacology and Pathology, School of Medicine, Wayne State University, Detroit, Michigan 48201-2013, USA.
Xuejun WangState Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Departments of Pathophysiology and Biochemistry, Guangzhou Medical University, Guangdong 510182, China; Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion, South Dakota 57069, USA.
Jinbao LiuState Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Departments of Pathophysiology and Biochemistry, Guangzhou Medical University, Guangdong 510182, China.
Guangzhou Medical University · CNSecond Affiliated Hospital of Guangzhou Medical University · CNState Key Laboratory of Oncology in South ChinaThe University of Texas MD Anderson Cancer Center · USUniversity of South Dakota · US

Funding

Ubiquitin receptors and cardiac proteotoxicityR01HL072166 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI WANG, XUEJUN · 2003 to 2023
$6.9M
The COP9 SIgnalosome in the HeartR01HL085629 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI WANG, XUEJUN · 2006 to 2019
$4.7M
(PQA1) Regulation of Metformin Response by Breast Cancer Associated Gene 2 (BCA2)R21CA184788 · NCI · WAYNE STATE UNIVERSITY · PI DOU, QING PING · 2014 to 2015
$364k
NCI NIH HHS R21 CA184788NHLBI NIH HHS HL072166NHLBI NIH HHS HL085629NHLBI NIH HHS R01 HL072166NHLBI NIH HHS R01 HL085629
6 · The paper itself

Abstract

Resistance to Imatinib mesylate (IM) is an emerging problem for patients with chronic myelogenous leukemia (CML). T315I mutation in the Bcr-Abl is the predominant mechanism of the acquired resistance to IM and second generation tyrosine kinase inhibitors (TKI). Therefore it is urgent to search for new measures to overcome TKI-resistance. Auranofin (AF), clinically used to treat rheumatic arthritis, was recently approved by US Food and Drug Administration for Phase II clinical trial to treat cancer. In contrast to the reports that AF induces apoptosis by increasing intracellular reactive oxygen species (ROS) levels via inhibiting thioredoxin reductase, our recent study revealed that AF-induced apoptosis depends on inhibition of proteasomal deubiquitinases (UCHL5 and USP14). Here we report that (i) AF induces apoptosis in both Bcr-Abl wild-type cells and Bcr-Abl-T315I mutation cells and inhibits the growth of IM-resistant Bcr-Abl-T315I xenografts in vivo; (ii) AF inhibits Bcr-Abl through both downregulation of Bcr-Abl gene expression and Bcr-Abl cleavage mediated by proteasome inhibition-induced caspase activation; (iii) proteasome inhibition but not ROS is required for AF-induced caspase activation and apoptosis. These findings support that AF overcomes IM resistance through both Bcr/Abl-dependent and -independent mechanisms, providing great clinical significance for cancer treatment.

Indexed as

AnimalsAntineoplastic AgentsAntirheumatic AgentsApoptosisAuranofinBenzamidesCell Line, TumorCell SurvivalDrug Resistance, NeoplasmFusion Proteins, bcr-ablHumansImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMiceMice, Inbred BALB CMice, NudeAntineoplastic AgentsAntirheumatic AgentsAuranofinBenzamidesFusion Proteins, bcr-ablImatinib MesylatePiperazinesProtein Kinase InhibitorsPyrimidinesReactive Oxygen SpeciesThioredoxin-Disulfide ReductaseUbiquitin ThiolesteraseUCHL5 protein, humanUSP14 protein, human

Identifiers

PMID25193854
PMCPMC4253423
OpenAlexW1890902147

What OpenQuestion holds

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Registered trials

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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.