Evidence map›Paper›PMID 34353343›Full record

ArticleJournal of translational medicine2021

E3 ubiquitin ligase TRIM29 promotes pancreatic cancer growth and progression via stabilizing Yes-associated protein 1.

Xueqiang Deng, Xiaowei Fu, Hong Teng, Lu Fang, Bo Liang, Rengui Zeng, Lian Chen, Yeqing Zou

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2021. 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
1.8field-weighted citation impact, top 16% 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, 24 citations in OpenAlex.

  1. Article
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  12. Ubiquitin signaling in pancreatic ductal adenocarcinoma.Frontiers in molecular biosciences · 2023
    Review
  13. E3 ubiquitin ligaseWorld journal of gastrointestinal oncology · 2022
    Article
  14. Review
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 3 institutions in 1 country.

Xueqiang Deng *Department of Orthopedics, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Xiaowei Fu *Department of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Hong TengJiangxi Province Key Laboratory of Molecular Medicine, The Second Affiliated Hospital of Nanchang University, 1 Minde Road, Nanchang, 330006, Jiangxi, China.
Lu FangDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Bo LiangDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Rengui ZengDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Lian ChenDepartment of Medical Ultrasonics, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China. zouyeqing3366@163.com.
Yeqing ZouJiangxi Province Key Laboratory of Molecular Medicine, The Second Affiliated Hospital of Nanchang University, 1 Minde Road, Nanchang, 330006, Jiangxi, China. zouyeqing3366@163.com.
Second Affiliated Hospital of Nanchang University · CNNanchang University · CNFirst Affiliated Hospital of Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPancreatic cancer (PC) is one of the most fatal digestive system cancers. tripartite motif-29 (TRIM29) has been reported as oncogene in several human cancers. However, the precise role and underlying signal cascade of TRIM29 in PC progression remain unclear.

methodsWestern blot, qRT-PCR and immunohistochemistry were used to analyze TRIM29 and Yes-associated protein 1 (YAP1) levels. CCK8 assays, EdU assays and flow cytometry were designed to explore the function and potential mechanism of TRIM29 and YAP1 in the proliferation of PC. Next, a nude mouse model of PC was established for validating the roles of TRIM29 and YAP1 in vivo. The relationship among TRIM29 and YAP1 was explored by co-immunoprecipitation and in vitro ubiquitination assay.

resultsTRIM29 and YAP1 was significantly upregulated in PC patient samples, and TRIM29 expression was closely related to a malignant phenotype and poorer overall survival (OS) of PC patients. Functional assays revealed that TRIM29 knockdown suppresses cell growth, arrests cell cycle progression and promotes cell apoptosis of PC cells in vivo and in vitro. Furthermore, the rescue experiments demonstrated that TRIM29-induced proliferation is dependent on YAP1 in PC cells. Mechanistically, TRIM29 regulates YAP1 expression by directly binding to YAP1, and reduced its ubiquitination and degradation.

conclusionTaken together, these results identify a novel mechanism used by PC growth, and provide insight regarding the role of TRIM29 in PC.

Indexed as

DNA-Binding ProteinsPancreatic NeoplasmsAnimalsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMiceTranscription FactorsUbiquitin-Protein LigasesDNA-Binding ProteinsTranscription FactorsTRIM29 protein, humanUbiquitin-Protein LigasesCell apoptosisCell cyclePancreatic cancerProliferationTRIM29YAP1

Identifiers

PMID34353343
PMCPMC8340474
OpenAlexW3165632314

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.