Evidence map›Paper›PMID 28682311›Full record

ArticleCell death & disease2017

Platinum pyrithione induces apoptosis in chronic myeloid leukemia cells resistant to imatinib via DUB inhibition-dependent caspase activation and Bcr-Abl downregulation.

Xiaoying Lan, Chong Zhao, Xin Chen, Peiquan Zhang, Dan Zang, Jinjie Wu, Jinghong Chen, Huidan Long, Li Yang, Hongbiao Huang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.2field-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

14 citing papers in PubMed, 21 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

13 authors at 2 institutions in 2 countries.

Xiaoying LanProtein Modification and Degradation Lab, SKLRD, School of Basic Medical Sciences, The affiliated Tumor Hospital of Guangzhou Medical University, Guangdong 511436, China.
Chong ZhaoProtein Modification and Degradation Lab, SKLRD, School of Basic Medical Sciences, The affiliated Tumor Hospital of Guangzhou Medical University, Guangdong 511436, China.
Xin ChenProtein Modification and Degradation Lab, SKLRD, School of Basic Medical Sciences, The affiliated Tumor Hospital of Guangzhou Medical University, Guangdong 511436, China.
Peiquan ZhangProtein Modification and Degradation Lab, SKLRD, School of Basic Medical Sciences, The affiliated Tumor Hospital of Guangzhou Medical University, Guangdong 511436, China.
Dan ZangProtein Modification and Degradation Lab, SKLRD, School of Basic Medical Sciences, The affiliated Tumor Hospital of Guangzhou Medical University, Guangdong 511436, China.
Jinjie WuProtein Modification and Degradation Lab, SKLRD, School of Basic Medical Sciences, The affiliated Tumor Hospital of Guangzhou Medical University, Guangdong 511436, China.
Jinghong ChenProtein Modification and Degradation Lab, SKLRD, School of Basic Medical Sciences, The affiliated Tumor Hospital of Guangzhou Medical University, Guangdong 511436, China.
Huidan LongProtein Modification and Degradation Lab, SKLRD, School of Basic Medical Sciences, The affiliated Tumor Hospital of Guangzhou Medical University, Guangdong 511436, China.
Li YangProtein Modification and Degradation Lab, SKLRD, School of Basic Medical Sciences, The affiliated Tumor Hospital of Guangzhou Medical University, Guangdong 511436, China.
Hongbiao HuangProtein Modification and Degradation Lab, SKLRD, School of Basic Medical Sciences, The affiliated Tumor Hospital of Guangzhou Medical University, Guangdong 511436, China.
Xuejun WangProtein Modification and Degradation Lab, SKLRD, School of Basic Medical Sciences, The affiliated Tumor Hospital of Guangzhou Medical University, Guangdong 511436, China.
Xianping ShiProtein Modification and Degradation Lab, SKLRD, School of Basic Medical Sciences, The affiliated Tumor Hospital of Guangzhou Medical University, Guangdong 511436, China.
Jinbao LiuProtein Modification and Degradation Lab, SKLRD, School of Basic Medical Sciences, The affiliated Tumor Hospital of Guangzhou Medical University, Guangdong 511436, China.
Guangzhou Medical University · CNUniversity of South Dakota · US

Funding

The COP9 SIgnalosome in the HeartR01HL085629 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI WANG, XUEJUN · 2006 to 2019
$4.7M
NHLBI NIH HHS R01 HL085629
6 · The paper itself

Abstract

Chronic myelogenous leukemia (CML) is characterized by the chimeric tyrosine kinase Bcr-Abl. T315I Bcr-Abl is the most notorious point mutation to elicit acquired resistance to imatinib (IM), leading to poor prognosis. Therefore, it is urgent to search for additional approaches and targeting strategies to overcome IM resistance. We recently reported that platinum pyrithione (PtPT) potently inhibits the ubiquitin-proteasome system (UPS) via targeting the 26 S proteasome-associated deubiquitinases (DUBs), without effecting on the 20 S proteasome. Here we further report that (i) PtPT induces apoptosis in Bcr-Abl wild-type and Bcr-Abl-T315I mutation cells including the primary mononuclear cells from CML patients clinically resistant to IM, as well as inhibits the growth of IM-resistant Bcr-Abl-T315I xenografts in vivo; (ii) PtPT downregulates Bcr-Abl level through restraining Bcr-Abl transcription, and decreasing Bcr-Abl protein mediated by DUBs inhibition-induced caspase activation; (iii) UPS inhibition is required for PtPT-induced caspase activation and cell apoptosis. These findings support that PtPT overcomes IM resistance through both Bcr-Abl-dependent and -independent mechanisms. We conclude that PtPT can be a lead compound for further drug development to overcome imatinib resistance in CML patients.

Indexed as

Gene Expression Regulation, LeukemicAnimalsAntineoplastic AgentsApoptosisBortezomibCaspasesCell Line, TumorCell ProliferationDeubiquitinating EnzymesDrug Resistance, NeoplasmFemaleFusion Proteins, bcr-ablHumansImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveLeukocytes, MononuclearAntineoplastic AgentsATP dependent 26S proteaseBCR-ABL1 fusion protein, humanBortezomibCaspasesDeubiquitinating EnzymesFusion Proteins, bcr-ablImatinib MesylateOrganoplatinum Compoundsplatinum pyrithioneProteasome Endopeptidase ComplexProteasome InhibitorsPyridines

Identifiers

PMID28682311
PMCPMC5550844
OpenAlexW2724983794

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.