Evidence map›Paper›PMID 26527005›Full record

ArticleCell reports2015

SPOP E3 Ubiquitin Ligase Adaptor Promotes Cellular Senescence by Degrading the SENP7 deSUMOylase.

Hengrui Zhu, Shancheng Ren, Benjamin G Bitler, Katherine M Aird, Zhigang Tu, Emmanuel Skordalakes, Yasheng Zhu, Jun Yan, Yinghao Sun, Rugang Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

44 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Molecular insights for the tumor suppressor role of SPOP in prostate cancer.Biochimica et biophysica acta. Reviews on cancer · 2026
    Review
  5. Article
  6. Article
  7. Degrons: defining the rules of protein degradation.Nature reviews. Molecular cell biology · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. The impact of dysregulation SUMOylation on prostate cancer.Journal of translational medicine · 2025
    Review
  12. Review
  13. Article
  14. The SUMOylation and ubiquitination crosstalk in cancer.Journal of cancer research and clinical oncology · 2023
    Review
  15. Article
  16. Review
  17. Article
  18. Cancer-Associated Dysregulation of Sumo Regulators: Proteases and Ligases.International journal of molecular sciences · 2022
    Review
  19. Article
  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

10 authors at 4 institutions in 2 countries.

Hengrui ZhuGene Expression and Regulation Program, The Wistar Institute, Philadelphia, PA 19104, USA.
Shancheng RenDepartment of Urology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai 200433, People's Republic of China.
Benjamin G BitlerGene Expression and Regulation Program, The Wistar Institute, Philadelphia, PA 19104, USA.
Katherine M AirdGene Expression and Regulation Program, The Wistar Institute, Philadelphia, PA 19104, USA.
Zhigang TuGene Expression and Regulation Program, The Wistar Institute, Philadelphia, PA 19104, USA.
Emmanuel SkordalakesGene Expression and Regulation Program, The Wistar Institute, Philadelphia, PA 19104, USA.
Yasheng ZhuDepartment of Urology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai 200433, People's Republic of China.
Jun YanMOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing University, Nanjing, Jiangsu 210061, People's Republic of China.
Yinghao SunDepartment of Urology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai 200433, People's Republic of China. Electronic address: sunyh@medmail.com.cn.
Rugang ZhangGene Expression and Regulation Program, The Wistar Institute, Philadelphia, PA 19104, USA. Electronic address: rzhang@wistar.org.
The Wistar Institute · USSecond Military Medical University · CNChanghai Hospital · CNModel Animal Research Center · CN

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Aaron Robert Goldman · 1985 to 2026
$75.9M
TRAINING PROGRAM IN BASIC CANCER RESEARCHT32CA009171 · NCI · WISTAR INSTITUTE · PI Alessandro Gardini · 1985 to 2026
$15.3M
Targeted Combination Therapy for MelanomaP50CA174523 · NCI · WISTAR INSTITUTE · PI HERLYN, MEENHARD F · 2014 to 2018
$11.1M
Role of BRCA1 Pathway in Regulating Oncogene-Induced SenescenceR01CA160331 · NCI · WISTAR INSTITUTE · PI ZHANG, RUGANG · 2012 to 2021
$4.0M
Targeting EZH2 in CARM1-expressing epithelial ovarian cancerR01CA163377 · NCI · WISTAR INSTITUTE · PI ZHANG, RUGANG · 2012 to 2021
$3.7M
Structural and Biochemical Analysis of Telomerase FunctionR01GM088332 · NIGMS · WISTAR INSTITUTE · PI SKORDALAKES, EMMANUEL · 2010 to 2014
$1.7M
Nucleotide Metabolism in Senescence and Platinum Resistance of Ovarian CancerR00CA194309 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI AIRD, KATHERINE MARIE · 2017 to 2019
$697k
Nucleotide Metabolism in Senescence and Platinum Resistance of Ovarian CancerK99CA194309 · NCI · WISTAR INSTITUTE · PI AIRD, KATHERINE MARIE · 2015 to 2016
$230k
Targeting Wnt signaling to overcome PARP inhibitor resistance in ovarian cancerK99CA194318 · NCI · WISTAR INSTITUTE · PI BITLER, BENJAMIN G · 2015 to 2016
$230k
NCI NIH HHS CA010815NCI NIH HHS K99 CA194309NCI NIH HHS K99CA194309NCI NIH HHS K99 CA194318NCI NIH HHS K99CA194318NCI NIH HHS P30 CA010815NCI NIH HHS P50 CA174523NCI NIH HHS R00 CA194309NCI NIH HHS R01 CA160331NCI NIH HHS R01CA160331NCI NIH HHS R01 CA163377NCI NIH HHS R01CA163377NCI NIH HHS T32 CA009171NCI NIH HHS T32CA9171-35NIGMS NIH HHS R01 GM088332
6 · The paper itself

Abstract

The SPOP gene, which encodes an E3 ubiquitin ligase adaptor, is frequently mutated in a number of cancer types. However, the mechanisms by which SPOP functions as a tumor suppressor remain poorly understood. Here, we show that SPOP promotes senescence, an important tumor suppression mechanism, by targeting the SENP7 deSUMOylase for degradation. SPOP is upregulated during senescence. This correlates with ubiquitin-mediated degradation of SENP7, which promotes senescence by increasing HP1α sumoylation and the associated epigenetic gene silencing. Ectopic wild-type SPOP, but not its cancer-associated mutants, drives senescence. Conversely, SPOP knockdown overcomes senescence. These phenotypes correlate with ubiquitination and degradation of SENP7 and HP1α sumoylation, subcellular re-localization, and its associated gene silencing. Furthermore, SENP7 is expressed at higher levels in prostate tumor specimens with SPOP mutation (n = 13) compared to those with wild-type SPOP (n = 80). In summary, SPOP acts as a tumor suppressor by promoting senescence through degrading SENP7.

Indexed as

Amino Acid SequenceCells, CulturedCellular SenescenceChromobox Protein Homolog 5EndopeptidasesGene SilencingHEK293 CellsHumansMaleMolecular Sequence DataNuclear ProteinsProstatic NeoplasmsProteolysisRepressor ProteinsSumoylationCBX5 protein, humanChromobox Protein Homolog 5EndopeptidasesNuclear ProteinsRepressor ProteinsSENP7 protein, humanSPOP protein, human

Identifiers

PMID26527005
PMCPMC4644472
OpenAlexW2184978240

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.