Evidence map›Paper›PMID 38240906›Full record

ArticleScience China. Life sciences2024

SUB1 promotes colorectal cancer metastasis by activating NF-κB signaling via UBR5-mediated ubiquitination of UBXN1.

Hao Wang, Wenwen Chen, Yanting Wang, Yuzhen Gao, Zizhen Zhang, Shuyi Mi, Liangjing Wang, Meng Xue

Abstract read
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In one paragraph

Article in Science China. Life sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

9 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. MicroRNA-582-5p modulation of UBR5 affects inflammatory response and motor recovery after spinal cord injury.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 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 4 institutions in 1 country.

Hao Wang *Department of Gastroenterology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, 310009, China.
Wenwen Chen *Department of Gastroenterology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, 310009, China.
Yanting Wang *Department of Gastroenterology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, 310009, China.
Yuzhen GaoDepartment of Clinical Laboratory, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, 310016, China.
Zizhen ZhangDepartment of Gastrointestinal Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital and Institute, Beijing, 100142, China.
Shuyi MiDepartment of Gastroenterology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, 310009, China.
Liangjing WangDepartment of Gastroenterology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, 310009, China. wangljzju@zju.edu.cn.
Meng XueDepartment of Gastroenterology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, 310009, China. xuemeng@zju.edu.cn.
Second Affiliated Hospital of Zhejiang University · CNPeking University · CNSir Run Run Shaw Hospital · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis accounts for the major cause of colorectal cancer (CRC) related mortality due to the lack of effective treatments. In this study, we integrated the single-cell RNA-seq (scRNA-seq) and bulk RNA-seq data and identified the transcriptional coactivator SUB1 homolog (Sac-Saccharomyces cerevisiae)/PC4 (positive cofactor 4) associated with CRC metastasis. Elevated SUB1 expression was correlated with advanced tumor stage and poor survival in CRC. In vivo and vitro assays showed that SUB1 depletion could inhibit the invasive and metastatic abilities of CRC cells. SUB1 activated NF-κB signaling and its transcriptional target genes CXCL1 and CXCL3 to drive CRC metastasis. Mechanistically, SUB1 integrated with the E3 ubiquitin-protein ligase UBR5 and increased its protein level in CRC cells. Subsequently, the increased UBR5 mainly mediated Lys11-linked polyubiquitination and degradation of NF-κB negative regulator UBXN1, thus to activate the NF-κB signaling. Overall, our study demonstrated that SUB1 promoted CRC progression by modulating UBR5/UBXN1 and activating NF-κB signaling, providing a new therapeutic strategy for treating metastatic CRC through targeting SUB1.

Indexed as

Colorectal NeoplasmsDNA-Binding ProteinsNF-kappa BSignal TransductionUbiquitinationUbiquitin-Protein LigasesAdaptor Proteins, Signal TransducingAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeNeoplasm MetastasisAdaptor Proteins, Signal TransducingDNA-Binding ProteinsNF-kappa BSUB1 protein, humanTranscription FactorsUbiquitin-Protein LigasesUBR5 protein, humanUBXN1 protein, humancolorectal cancerMetastasisNF-κB signalingSUB1UBR5

Identifiers

PMID38240906
OpenAlexW4391032044

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.