Evidence map›Paper›PMID 41707797›Full record

ReviewBiochimica et biophysica acta. Reviews on cancer2026

Molecular insights for the tumor suppressor role of SPOP in prostate cancer.

Peiqiang Yan, Xutong Xue, Tao Hou, Jingchao Wang, Weiwei Jiang, Zhen Wang, Hiroyuki Inuzuka, Wenyi Wei

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Biochimica et biophysica acta. Reviews on cancer, 2026. 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
–field-weighted citation impact
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.

  1. Review
  2. 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

8 authors.

Peiqiang YanDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.
Xutong XueDepartment of Neurology & F.M. Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Tao HouDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.
Jingchao WangDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.
Weiwei JiangDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.
Zhen WangDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.
Hiroyuki InuzukaDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.
Wenyi WeiDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA. Electronic address: wwei2@bidmc.harvard.edu.

Funding

Deciphering the physiological role and interplay between ubiquitination and phosphorylation pathways to guide targeted cancer therapiesR35CA253027 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Wenyi Wei · 2020 to 2026
$6.2M
Targeting the SKP2 Axis for Anti-melanoma TherapyR01CA291991 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Hiroyuki Inuzuka · 2025 to 2026
$791k
NCI NIH HHS R01 CA291991NCI NIH HHS R35 CA253027
6 · The paper itself

Abstract

Speckle-type POZ protein (SPOP) functions as a substrate adaptor within the cullin 3-based E3 ubiquitin ligase complex, playing an essential role in regulating diverse cellular processes by targeting specific proteins toward ubiquitination and proteasomal degradation. Aberrations in SPOP-driven proteolytic pathways have been implicated in the initiation and progression of prostate cancer. In this context, SPOP appears to function largely as a tumor suppressor by mediating the degradation of several oncogenic proteins such as AR, SRC3, CDC20, MYC, ERG, PD-L1, and BRD4. Mutations that impair SPOP function can result in the promotion of these substrates' oncogenic function, contributing to tumor initiation and progression. Hence, a deeper investigation into the molecular mechanisms of SPOP in prostate cancer will provide novel insights into its physiological function in oncogenesis and drug development. In this review, we summarize SPOP's tumor suppressor functions and structural features, upstream regulatory mechanisms, and SPOP-targeting therapeutic strategies in prostate cancer.

Indexed as

Nuclear ProteinsProstatic NeoplasmsRepressor ProteinsAnimalsHumansMaleUbiquitinationNuclear ProteinsRepressor ProteinsSPOP protein, humanE3 ligaseProstate cancerProtein degradationSPOPTumor suppressorUbiquitination

Identifiers

PMID41707797
PMCPMC13338896

What Socratic holds

Textmetadata
LicenceTDM
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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.