Evidence map›Paper›PMID 33963175›Full record

ArticleCell death & disease2021

Suppression of USP7 induces BCR-ABL degradation and chronic myelogenous leukemia cell apoptosis.

Shuoyi Jiang, Xiaoge Wang, Yuanming He, Hongbiao Huang, Biyin Cao, Zubin Zhang, Jinbao Liu, Qi Wang, Zhenqian Huang, Xinliang Mao

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 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

10 authors at 4 institutions in 1 country.

Shuoyi Jiang *Department of Hematology, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, China.
Xiaoge Wang *Institute of Clinical Pharmacology, Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Yuanming HeGuangdong and Guangzhou Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, P. R. China.
Hongbiao HuangGuangdong and Guangzhou Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, P. R. China.ORCID 0000-0002-9873-0559
Biyin CaoDepartment of Pharmacology, Soochow University, Jiangsu, 215123, P. R. China.
Zubin ZhangDepartment of Pharmacology, Soochow University, Jiangsu, 215123, P. R. China.
Jinbao LiuGuangdong and Guangzhou Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, P. R. China.
Qi WangInstitute of Clinical Pharmacology, Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Zhenqian HuangDepartment of Hematology, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, China. huangzq2013@163.com.
Xinliang MaoDepartment of Hematology, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, China. xinliangmao@gzhmu.edu.cn.
Soochow University · CNGuangzhou University of Chinese Medicine · CNGuangzhou Medical University · CNFirst Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic myelogenous leukemia (CML) is a clonal malignancy of hematopoietic stem cells featured with the fusion protein kinase BCR-ABL. To elicit the mechanism underlying BCR-ABL stability, we perform a screen against a panel of deubiquitinating enzymes (DUBs) and find that the ubiquitin-specific protease 7 (USP7) drastically stabilizes the BCR-ABL fusion protein. Further studies show that USP7 interacts with BCR-ABL and blocks its polyubiquitination and degradation. Moreover, USP7 knockdown triggers BCR-ABL degradation and suppresses its downstream signaling transduction. In line with this finding, genetic or chemical inhibition of USP7 leads to BCR-ABL protein degradation, suppresses BCR/ABL signaling, and induces CML cell apoptosis. Furthermore, we find the antimalarial artesunate (ART) significantly inhibits USP7/BCR-ABL interaction, thereby promoting BCR-ABL degradation and inducing CML cell death. This study thus identifies USP7 as a putative Dub of BCR-ABL and provides a rationale in targeting USP7/BCR-ABL for the treatment of CML.

Indexed as

ApoptosisCell ProliferationFusion Proteins, bcr-ablHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveTransfectionUbiquitin-Specific Peptidase 7Fusion Proteins, bcr-ablUbiquitin-Specific Peptidase 7USP7 protein, human

Identifiers

PMID33963175
PMCPMC8105359
OpenAlexW3159744286

What Socratic holds

Textmetadata
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 Socratic graph.