Evidence map›Paper›PMID 39922805›Full record

ArticleCell death & disease2025

USP4-mediated CENPF deubiquitylation regulated tumor metastasis in colorectal cancer.

Zhongdong Xie, Hanbin Lin, Yuecheng Wu, Yanan Yu, Xintong Liu, Yating Zheng, Xiaojie Wang, Jiashu Wu, Meifang Xu, Yuting Han and 8 more

Abstract read
In one paragraph

Article in Cell death & disease, 2025. 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. Article
  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

18 authors.

Zhongdong Xie *Department of Colorectal Surgery, Union Hospital, Fujian Medical University, Fuzhou, China.
Hanbin Lin *Central Laboratory, Affiliated Hospital of Putian University, Putian, China.ORCID http://orcid.org/0000-0002-1290-415X
Yuecheng Wu *Key Laboratory of Gastrointestinal Cancer (Fujian Medical University), Ministry of Education, Fuzhou, China.
Yanan Yu *Guilin Medical University, Guilin, China.
Xintong Liu *Central Laboratory, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Yating ZhengDepartment of Colorectal Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Xiaojie WangDepartment of Colorectal Surgery, Union Hospital, Fujian Medical University, Fuzhou, China.
Jiashu WuDepartment of Science and Technology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Meifang XuDepartment of Pathology, Union Hospital, Fujian Medical University, Fuzhou, China.
Yuting HanKey Laboratory of Gastrointestinal Cancer (Fujian Medical University), Ministry of Education, Fuzhou, China.
Qiongying ZhangDepartment of Pathology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Yu DengDepartment of Colorectal Surgery, Union Hospital, Fujian Medical University, Fuzhou, China.
Lin LinDepartment of Pathology, Union Hospital, Fujian Medical University, Fuzhou, China.
Yan LinzhuDepartment of Colorectal Surgery, Union Hospital, Fujian Medical University, Fuzhou, China.
Li QingyunDepartment of Colorectal Surgery, Union Hospital, Fujian Medical University, Fuzhou, China.
Xinjian LinKey Laboratory of Gastrointestinal Cancer (Fujian Medical University), Ministry of Education, Fuzhou, China. xlin@fjmu.edu.cn.
Ying HuangDepartment of Colorectal Surgery, Union Hospital, Fujian Medical University, Fuzhou, China. fjxhhy@sina.com.
Pan ChiDepartment of Colorectal Surgery, Union Hospital, Fujian Medical University, Fuzhou, China. chipanfjxh@163.com.ORCID http://orcid.org/0009-0002-2663-2252

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis is a major challenge for colorectal cancer (CRC) treatment. In this study, we identified autophagy activation as a prognostic indicator in CRC and observed that the expression of key autophagy proteins is elevated in metastatic and recurrent cases. Our subsequent goal was to identify potential genes associated with the autophagy panel and assess their prognostic significance, biological roles, and mechanisms in CRC metastasis. Among the candidates, CENPF emerged as the top gene in our screening process. We found that CENPF expression was preferentially elevated in CRC tissues compared to adjacent normal tissues, with significantly higher levels in CRC patients with tumor recurrence. Furthermore, a multicenter cohort study demonstrated that upregulated CENPF expression was strongly associated with poorer disease-free survival in CRC. Functional experiments showed that CENPF knockdown inhibited CRC cell invasion and metastasis both in vitro and in vivo. Intriguingly, we found CENPF undergoes degradation in CRC via the ubiquitination-proteasome pathway. Mechanistically, we observed that USP4 interacted with and stabilized CENPF via deubiquitination. Furthermore, USP4-mediated CENPF upregulation was critical regulators of metastasis of CRC. Examination of clinical samples confirmed that USP4 expression positively correlates with CENPF protein expression, but not mRNA transcript levels. Taken together, this study describes a novel USP4-CENPF signaling axis which is crucial for CRC metastasis, potentially serving as a therapeutic target and a promising prognostic biomarker for CRC.

Indexed as

Colorectal NeoplasmsUbiquitin-Specific ProteasesAnimalsAutophagyCell Line, TumorCell MovementChromosomal Proteins, Non-HistoneFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred BALB CMice, NudeMicrofilament ProteinsNeoplasm Invasivenesscentromere protein FChromosomal Proteins, Non-HistoneMicrofilament ProteinsUbiquitin-Specific ProteasesUSP4 protein, human

Identifiers

PMID39922805
PMCPMC11807140

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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.