Evidence map›Paper›PMID 40119906›Full record

ArticleEuropean archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery2025

AGR2 activates the TGF-β/Smad signaling pathway to promote epithelial-mesenchymal transition, invasion, and metastasis in nasopharyngeal carcinoma.

Hui Jin, Gengtian Liang, Wenxia Huang, Zhen Wang, Longjun Wu, Yaping Li

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Article in European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery, 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. 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

6 authors.

Hui JinDepartment of Otolaryngology, Wuhan Third Hospital, No. 241 Pengliuyang Road, Wuchang District, Wuhan City, 430000, Hubei Province, China.
Gengtian LiangDepartment of Otolaryngology, Wuhan Third Hospital, No. 241 Pengliuyang Road, Wuchang District, Wuhan City, 430000, Hubei Province, China. gtliang_1sr@163.com.ORCID http://orcid.org/0009-0009-8655-7443
Wenxia HuangDepartment of Otolaryngology, Wuhan Third Hospital, No. 241 Pengliuyang Road, Wuchang District, Wuhan City, 430000, Hubei Province, China.
Zhen WangDepartment of Otolaryngology, Wuhan Third Hospital, No. 241 Pengliuyang Road, Wuchang District, Wuhan City, 430000, Hubei Province, China.
Longjun WuDepartment of Otolaryngology, Wuhan Third Hospital, No. 241 Pengliuyang Road, Wuchang District, Wuhan City, 430000, Hubei Province, China.
Yaping LiDepartment of Cardiology, Wuhan Third Hospital, Wuhan, 430000, Hubei Province, China.

Funding

The Fundding for Scientific Research Projects from Wuhan Municipal Heaith Commission WX23Z04
6 · The paper itself

Abstract

backgroundAnterior gradient 2 protein (AGR2) is associated with tumorigenesis and metastasis in different cancers. However, its role in nasopharyngeal carcinoma (NPC) remains unknown. This study aimed to explore the effect of AGR2 on epithelial-mesenchymal transition (EMT) in NPC and its underlying mechanisms.

methodsAGR2 expression was analyzed in cancerous and para-cancerous tissues from ten NPC patients using RT-qPCR. Western blotting was used to determine the AGR2 protein levels in two NPC cell lines and a nasopharyngeal epithelial cell line. AGR2 was overexpressed or knocked out in NPC cells and its effects on cell viability, migration, invasion, and EMT markers were evaluated in vitro.

resultAGR2 expression was significantly higher in NPC tissues compared to adjacent normal tissues. Similarly, NPC cell lines exhibited increased AGR2 levels compared to the nasopharyngeal epithelial cell line. AGR2 knockout significantly reduced cell viability, migration, and invasion. It also decreased N-cadherin protein levels while increasing E-cadherin, α-SMA, and vimentin expression. Conversely, AGR2 overexpression produced the opposite effects. Furthermore, AGR2 deletion inactivated the TGF-β/Smad signaling pathway.

conclusionAGR2 promotes tumor progression and EMT in NPC through activation of the TGF-β/Smad signaling pathway. These findings suggest that AGR2 may serve as a potential biomarker and therapeutic target for NPC.

Indexed as

Epithelial-Mesenchymal TransitionMucoproteinsNasopharyngeal CarcinomaNasopharyngeal NeoplasmsSmad ProteinsTransforming Growth Factor betaCell Line, TumorCell MovementCell SurvivalFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedNeoplasm InvasivenessNeoplasm MetastasisAGR2 protein, humanMucoproteinsOncogene ProteinsSmad ProteinsTransforming Growth Factor betaAGR2EMTInvasionMigrationNasopharyngeal carcinomaTGF-β/Smad

Identifiers

What Socratic holds

Textmetadata
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Registered trials

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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 Socratic graph.