Evidence map›Paper›PMID 36042498›Full record

ArticleJournal of translational medicine2022

SPOP promotes cervical cancer progression by inducing the movement of PD-1 away from PD-L1 in spatial localization.

Jiangchun Wu, Yong Wu, Qinhao Guo, Siyu Chen, Simin Wang, Xiaohua Wu, Jun Zhu, Xingzhu Ju

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

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  3. Molecular insights for the tumor suppressor role of SPOP in prostate cancer.Biochimica et biophysica acta. Reviews on cancer · 2026
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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

8 authors at 2 institutions in 1 country.

Jiangchun Wu *Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Yong Wu *Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Qinhao Guo *Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Siyu ChenDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Simin WangDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Xiaohua Wu *Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China. wu.xh@fudan.edu.cn.
Jun Zhu *Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China. joelchu88@qq.com.
Xingzhu Ju *Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China. xingzhu_ju@163.com.
Fudan University Shanghai Cancer Center · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMetastasis is a major obstacle in the treatment of cervical cancer (CC), and SPOP-mediated regulatory effects are involved in metastasis. However, the mechanisms have not been fully elucidated.

methodsProteomic sequencing and SPOP immunohistochemistry (IHC) were performed for the pelvic lymph node (pLN)-positive and non-pLN groups of CC patients. The corresponding patients were stratified by SPOP expression level for overall survival (OS) and relapse-free survival (RFS) analysis. In vitro and in vivo tests were conducted to verify the causal relationship between SPOP expression and CC metastasis. Multiplex immunofluorescence (m-IF) and the HALO system were used to analyse the mechanism, which was further verified by in vitro experiments.

resultsSPOP is upregulated in CC with pLN metastasis and negatively associated with patient outcome. In vitro and in vivo, SPOP promotes CC proliferation and metastasis. According to m-IF and HALO analysis, SPOP may promote CC metastasis by promoting the separation of PD-1 from PD-L1. Finally, it was further verified that SPOP can achieve immune tolerance by promoting the movement of PD-1 away from PD-L1 in spatial location and function.

conclusionThis study shows that SPOP can inhibit the immune microenvironment by promoting the movement of PD-1 away from PD-L1, thereby promoting pLN metastasis of CC and resulting in worse OS and RFS.

Indexed as

B7-H1 AntigenUterine Cervical NeoplasmsFemaleHumansLymphatic MetastasisNeoplasm Recurrence, LocalNuclear ProteinsProgrammed Cell Death 1 ReceptorProteomicsRepressor ProteinsTumor MicroenvironmentB7-H1 AntigenNuclear ProteinsProgrammed Cell Death 1 ReceptorRepressor ProteinsSPOP protein, humanCervical cancerCXCL16/CXCR6 axisMultiplex immunofluorescencePD-1/PD-L1 axisSPOP

Identifiers

PMID36042498
PMCPMC9429754
OpenAlexW4293567336

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.