Evidence map›Paper›PMID 27958289›Full record

ArticleCell research2017

WSB1 overcomes oncogene-induced senescence by targeting ATM for degradation.

Jung Jin Kim, Seung Baek Lee, Sang-Yeop Yi, Sang-Ah Han, Sun-Hyun Kim, Jong-Min Lee, Seo-Yun Tong, Ping Yin, Bowen Gao, Jun Zhang and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.6field-weighted citation impact, top 26% 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

26 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
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  4. WSB1 is dispensable for mouse spermatogenesis and male fertility.American journal of translational research · 2026
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  13. Genes · 2023
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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

11 authors at 4 institutions in 2 countries.

Jung Jin KimDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Seung Baek LeeDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Sang-Yeop YiDepartment of Medical Education, International St. Mary's Hospital, College of Medicine, Catholic Kwandong University, Incheon 404834, Republic of Korea.
Sang-Ah HanDepartment of Surgery, School of Medicine, Kyung Hee University, Seoul 130872, Republic of Korea.
Sun-Hyun KimDepartment of Family Medicine, International St. Mary's Hospital, College of Medicine, Catholic Kwandong University, Incheon 404834, Republic of Korea.
Jong-Min LeeDepartment of Obstetrics and Gynecology, School of Medicine, Kyung Hee University, Seoul 130872, Republic of Korea.
Seo-Yun TongDepartment of Obstetrics and Gynecology, School of Medicine, Kyung Hee University, Seoul 130872, Republic of Korea.
Ping YinDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Bowen GaoDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Jun ZhangDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN 55905, USA.
Zhenkun LouDepartment of Oncology, Mayo Clinic, Rochester, MN 55905, USA.
Mayo Clinic in Arizona · USKyung Hee University · KRCatholic Kwandong University International St. Mary's Hospital · KRWinnMed · US

Funding

Women's Cancer ProgramP30CA015083 · NCI · MAYO CLINIC ROCHESTER · PI AKHILESH PANDEY · 1985 to 2026
$151.3M
Ubiquitination and the DNA Damage Response PathwayR01CA130996 · NCI · MAYO CLINIC ROCHESTER · PI LOU, ZHENKUN · 2008 to 2018
$3.3M
Regulation of homologous recombination and cancer cell response to chemoradiotherapyR01CA203561 · NCI · MAYO CLINIC ROCHESTER · PI LOU, ZHENKUN · 2016 to 2020
$1.8M
The Role of WSB1 in TumorigenesisR01CA189666 · NCI · MAYO CLINIC ROCHESTER · PI LOU, ZHENKUN · 2014 to 2018
$1.6M
NCI NIH HHS P30 CA015083NCI NIH HHS R01 CA130996NCI NIH HHS R01 CA189666NCI NIH HHS R01 CA203561
6 · The paper itself

Abstract

Oncogene-induced senescence (OIS) or apoptosis through the DNA-damage response is an important barrier of tumorigenesis. Overcoming this barrier leads to abnormal cell proliferation, genomic instability, and cellular transformation, and finally allows cancers to develop. However, it remains unclear how the OIS barrier is overcome. Here, we show that the E3 ubiquitin ligase WD repeat and SOCS box-containing protein 1 (WSB1) plays a role in overcoming OIS. WSB1 expression in primary cells helps the bypass of OIS, leading to abnormal proliferation and cellular transformation. Mechanistically, WSB1 promotes ATM ubiquitination, resulting in ATM degradation and the escape from OIS. Furthermore, we identify CDKs as the upstream kinase of WSB1. CDK-mediated phosphorylation activates WSB1 by promoting its monomerization. In human cancer tissue and in vitro models, WSB1-induced ATM degradation is an early event during tumorigenic progression. We suggest that WSB1 is one of the key players of early oncogenic events through ATM degradation and destruction of the tumorigenesis barrier. Our work establishes an important mechanism of cancer development and progression in premalignant lesions.

Indexed as

Cellular SenescenceOncogenesProteolysisAnimalsAtaxia Telangiectasia Mutated ProteinsCarcinogenesisCell Transformation, NeoplasticHEK293 CellsHeLa CellsHumansIntracellular Signaling Peptides and ProteinsMiceModels, BiologicalPhosphorylationProtein BindingProtein DomainsAtaxia Telangiectasia Mutated ProteinsIntracellular Signaling Peptides and ProteinsProteinsUbiquitin-Protein LigasesWSB1 protein, humanWsb1 protein, mouse

Identifiers

PMID27958289
PMCPMC5339850
OpenAlexW2565255170

What OpenQuestion holds

Textmetadata
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.