Evidence map›Paper›PMID 29059170›Full record

ArticleOncogene2018

SPSB3 targets SNAIL for degradation in GSK-3β phosphorylation-dependent manner and regulates metastasis.

Y Liu, H Zhou, R Zhu, F Ding, Y Li, X Cao, Z Liu

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
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  6. American journal of translational research · 2025
    Article
  7. Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 2025
    Review
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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

7 authors at 2 institutions in 1 country.

Y LiuState Key Laboratory of Molecular Oncology, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, PR China.
H ZhouState Key Laboratory of Molecular Oncology, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, PR China.
R ZhuState Key Laboratory of Molecular Oncology, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, PR China.
F DingState Key Laboratory of Molecular Oncology, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, PR China.
Y LiState Key Laboratory of Molecular Oncology, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, PR China.
X CaoDepartment of Surgical Oncology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, PR China.
Z LiuState Key Laboratory of Molecular Oncology, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, PR China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) is a process during which normal epithelial cells acquire mesenchymal characteristics. EMT has a critical role in various human diseases especially in cancer. EMT facilitates tumor initiation and progression by mediating cancer cell stemness and motility. Zinc finger transcription factor SNAIL is one of the most important initiators of EMT. Therefore, it is of great significance to understand the regulating mechanism of SNAIL. In this study, we carried out a luciferase-based genome-wide screening using small interfering RNA library against ~200 of E3 ligases and ubiquitin-related genes and identified SOCS box protein SPSB3 as a novel E3 ligase component that targets SNAIL into polyubiquitination and degradation in response to GSK-3β phosphorylation of SNAIL. Functionally, we observed that SPSB3 overexpression greatly inhibits tumor metastasis by regulating SNAIL degradation both in vitro and in vivo. The expression of SPSB3 and SNAIL are negatively correlated in human esophageal squamous cell carcinoma tissues, and low SPSB3 expression indicates lymph node metastasis. Moreover, high SPSB3 expression indicates good survivals in various kinds of cancer. Collectively, these findings suggest that SPSB3-mediated SNAIL degradation has a vital role in regulating EMT and cancer progression.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsApoptosisBiomarkers, TumorCarcinoma, Squamous CellCase-Control StudiesCell MovementCell ProliferationEsophageal NeoplasmsFemaleFollow-Up StudiesGlycogen Synthase Kinase 3 betaHumansLymphatic MetastasisMiceMice, Inbred BALB CBiomarkers, TumorGlycogen Synthase Kinase 3 betaGSK3B protein, humanSNAI1 protein, humanSnail Family Transcription FactorsSPSB2 protein, humanSuppressor of Cytokine Signaling Proteins

Identifiers

PMID29059170
OpenAlexW2766250519

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.