Evidence map›Paper›PMID 34133717›Full record

ArticleNucleic acids research2021

Prostate cancer-associated SPOP mutations lead to genomic instability through disruption of the SPOP-HIPK2 axis.

Xiaofeng Jin, Shi Qing, Qian Li, Hui Zhuang, Liliang Shen, Jinhui Li, Honggang Qi, Ting Lin, Zihan Lin, Jian Wang and 12 more

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

Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Molecular insights for the tumor suppressor role of SPOP in prostate cancer.Biochimica et biophysica acta. Reviews on cancer · 2026
    Review
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  11. Review
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  14. Targeting PI3K/Akt signaling in prostate cancer therapy.Journal of cell communication and signaling · 2023
    Review
  15. Article
  16. Article
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  18. Review
  19. Review
  20. Article
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

22 authors at 3 institutions in 1 country.

Xiaofeng JinThe Affiliated Hospital of Medical School, Ningbo University, Ningbo 315020, China.ORCID 0000-0003-0801-8638
Shi QingState Key Lab of Genetic Engineering, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Fudan University, Shanghai 200438, China.
Qian LiThe Affiliated Hospital of Medical School, Ningbo University, Ningbo 315020, China.
Hui ZhuangThe Affiliated Hospital of Medical School, Ningbo University, Ningbo 315020, China.
Liliang ShenDepartment of Urology, Department of Hematology, the Affiliated Yinzhou Renmin Hospital of Medical School of Ningbo University, Ningbo 315040, China.
Jinhui LiThe Affiliated Hospital of Medical School, Ningbo University, Ningbo 315020, China.
Honggang QiDepartment of Urology, the Affiliated Yinzhou Second Hospital of Medical School of Ningbo University, Ningbo 315100, China.
Ting LinThe Affiliated Hospital of Medical School, Ningbo University, Ningbo 315020, China.
Zihan LinThe Affiliated Hospital of Medical School, Ningbo University, Ningbo 315020, China.
Jian WangThe Affiliated Hospital of Medical School, Ningbo University, Ningbo 315020, China.
Xinyi CaoThe Affiliated Hospital of Medical School, Ningbo University, Ningbo 315020, China.
Jianye YangThe Affiliated Hospital of Medical School, Ningbo University, Ningbo 315020, China.
Qi MaTranslational Research Laboratory for Urology, the Key Laboratory of Ningbo City. Ningbo First Hospital, The affiliated hospital of Ningbo University, Ningbo, Zhejiang 315010, China.
Linghua CongDepartment of Urology, Department of Hematology, the Affiliated Yinzhou Renmin Hospital of Medical School of Ningbo University, Ningbo 315040, China.
Yang XiDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo 315211, China.
Shuai FangDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo 315211, China.
Xiaodan MengDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo 315211, China.
Zhaohui GongDepartment of Biochemistry and Molecular Biology, Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo 315211, China.
Meng YeThe Affiliated Hospital of Medical School, Ningbo University, Ningbo 315020, China.
Shuyun WangDepartment of Breast Surgery, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 201204, China.
Chenji WangState Key Lab of Genetic Engineering, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Fudan University, Shanghai 200438, China.ORCID 0000-0002-5752-6439
Kun GaoDepartment of Clinical Laboratory, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 201204, China.
Ningbo University · CNFudan University · CNShanghai First Maternity and Infant Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Speckle-type Poz protein (SPOP), an E3 ubiquitin ligase adaptor, is the most frequently mutated gene in prostate cancer. The SPOP-mutated subtype of prostate cancer shows high genomic instability, but the underlying mechanisms causing this phenotype are still largely unknown. Here, we report that upon DNA damage, SPOP is phosphorylated at Ser119 by the ATM serine/threonine kinase, which potentiates the binding of SPOP to homeodomain-interacting protein kinase 2 (HIPK2), resulting in a nondegradative ubiquitination of HIPK2. This modification subsequently increases the phosphorylation activity of HIPK2 toward HP1γ, and then promotes the dissociation of HP1γ from trimethylated (Lys9) histone H3 (H3K9me3) to initiate DNA damage repair. Moreover, the effect of SPOP on the HIPK2-HP1γ axis is abrogated by prostate cancer-associated SPOP mutations. Our findings provide new insights into the molecular mechanism of SPOP mutations-driven genomic instability in prostate cancer.

Indexed as

Genomic InstabilityAtaxia Telangiectasia Mutated ProteinsCarrier ProteinsCell Line, TumorChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneDNA DamageHistonesHumansMaleMutationNuclear ProteinsPhosphorylationProstatic NeoplasmsProtein Serine-Threonine KinasesRepressor ProteinsAtaxia Telangiectasia Mutated ProteinsCarrier ProteinsChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneHIPK2 protein, humanHistonesNuclear ProteinsProtein Serine-Threonine KinasesRepressor ProteinsSerineSPOP protein, human

Identifiers

PMID34133717
PMCPMC8266658
OpenAlexW3172573923

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.