Evidence map›Paper›PMID 36257929›Full record

ArticleCell death discovery2022

The role of E3 ubiquitin ligase WWP2 and the regulation of PARP1 by ubiquitinated degradation in acute lymphoblastic leukemia.

Xinxin Lu, Xinyue Huang, Haiqi Xu, Saien Lu, Shilong You, Jiaqi Xu, Qianru Zhan, Chao Dong, Ning Zhang, Ying Zhang and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

2 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
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

14 authors at 3 institutions in 1 country.

Xinxin Lu *Department of Hematology, the First Hospital of China Medical University, Shenyang, Liaoning, China.
Xinyue Huang *Department of Cardiology, the First Hospital of China Medical University, Shenyang, Liaoning, China.ORCID http://orcid.org/0000-0001-8528-3465
Haiqi XuDepartment of Hematology, General Hospital of PLA Northern Theater Command, Shenyang, Liaoning, China.
Saien LuDepartment of Cardiology, the First Hospital of China Medical University, Shenyang, Liaoning, China.
Shilong YouDepartment of Cardiology, the First Hospital of China Medical University, Shenyang, Liaoning, China.
Jiaqi XuDepartment of Cardiology, the First Hospital of China Medical University, Shenyang, Liaoning, China.
Qianru ZhanDepartment of Hematology, the First Hospital of China Medical University, Shenyang, Liaoning, China.
Chao DongDepartment of Hematology, the First Hospital of China Medical University, Shenyang, Liaoning, China.
Ning ZhangDepartment of Hematology, the First Hospital of China Medical University, Shenyang, Liaoning, China.
Ying ZhangDepartment of Cardiology, the First Hospital of China Medical University, Shenyang, Liaoning, China.ORCID http://orcid.org/0000-0003-0962-7398
Liu CaoInstitute of Health Sciences, China Medical University, Shenyang, Liaoning, China.
Xingang ZhangDepartment of Cardiology, the First Hospital of China Medical University, Shenyang, Liaoning, China. zhangxingang80@aliyun.com.ORCID http://orcid.org/0000-0001-8811-1634
Naijin ZhangDepartment of Cardiology, the First Hospital of China Medical University, Shenyang, Liaoning, China. njzhang@cmu.edu.cn.ORCID http://orcid.org/0000-0003-3653-9801
Lijun ZhangDepartment of Hematology, the First Hospital of China Medical University, Shenyang, Liaoning, China. lzhang202003@163.com.ORCID http://orcid.org/0000-0002-9821-1863
First Hospital of China Medical University · CNChina Medical University · CNGeneral Hospital of Shenyang Military Region · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81800361National Natural Science Foundation of China (National Science Foundation of China) 81900355National Natural Science Foundation of China (National Science Foundation of China) 81900372National Natural Science Foundation of China (National Science Foundation of China) 81970211National Natural Science Foundation of China (National Science Foundation of China) 82171571National Natural Science Foundation of China (National Science Foundation of China) 82171572
6 · The paper itself

Abstract

Acute lymphoblastic leukemia (ALL) has been a huge threat for people's health and finding effective target therapy is urgent and important. WWP2, as one of E3 ubiquitin ligase, is involved in many biological processes by specifically binding to substrates. PARP1 plays a role in cell apoptosis and is considered as a therapeutic target of certain cancers. In this study, we firstly found that WWP2 expressed higher in newly diagnosed ALL patients comparing with complete remission (CR) ALL patients and normal control people, and WWP2 in relapse ALL patients expressed higher than normal control people. WWP2 expression was related with the FAB subtype of ALL and the proportion of blast cells in bone marrow blood tested by flow cytometry. We demonstrated knockout WWP2 inhibited the ALL growth and enhanced apoptosis induced by Dox in vitro and vivo for the first time. WWP2 negatively regulated and interacted with PARP1 and WWP2 mechanically degraded PARP1 through polyubiquitin-proteasome pathway in ALL. These findings suggested WWP2 played a role in ALL development as well as growth and apoptosis, and also displayed a regulatory pathway of PARP1, which provided a new potential therapeutic target for the treatment of ALL.

Identifiers

PMID36257929
PMCPMC9579143
OpenAlexW4306694408

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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.