Evidence map›Paper›PMID 40661947›Full record

ArticleFrontiers in immunology2025

LncRNA NEAT1 promotes epithelial-mesenchymal transition in nasal polyp cells via the miR-199-3p/PAK4 axis.

Shuman Li, Yu Jiang, Yalan Zhang, Bowen Zheng, Chao Yuan, Yang Shen, Yi Zhao, Tao Lu, Yucheng Yang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Shuman LiDepartment of Otorhinolaryngology, Upper Airway Inflammation and Tumor Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yu JiangDepartment of Otorhinolaryngology, Upper Airway Inflammation and Tumor Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yalan ZhangDepartment of Otorhinolaryngology, Upper Airway Inflammation and Tumor Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Bowen ZhengDepartment of Otorhinolaryngology, Upper Airway Inflammation and Tumor Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Chao YuanDepartment of Pediatrics, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, China.
Yang ShenDepartment of Otorhinolaryngology, Upper Airway Inflammation and Tumor Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yi ZhaoChongqing Key Laboratory of Translational Research for Cancer Metastasis and Individualized Treatment, Chongqing University Cancer Hospital, Chongqing, China.
Tao LuDepartment of Otorhinolaryngology, Upper Airway Inflammation and Tumor Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yucheng YangDepartment of Otorhinolaryngology, Upper Airway Inflammation and Tumor Laboratory, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and purpose: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a persistent inflammatory condition marked by high recurrence and limited therapeutic efficacy. This study investigates the role of long non-coding RNA NEAT1 in promoting epithelial-mesenchymal transition (EMT) in CRSwNP, focusing on its regulatory interaction with the miR-199-3p/PAK4 axis. Methods: NEAT1 expression was assessed in nasal epithelial cells from CRSwNP patients using qPCR and FISH. Primary human nasal epithelial cells and BEAS-2B cells were subjected to NEAT1 knockdown via siRNA. Cell migration, barrier function, and cytoskeletal dynamics were evaluated through scratch assays, Transwell migration, FITC-Dextran permeability testing, and phalloidin staining. EMT marker expression was analyzed via Western blotting and immunofluorescence. Transcriptome sequencing identified PAK4 as a downstream effector. Results: In comparison to controls, NEAT1 expression was significantly elevated in the epithelial tissues of CRSwNP. NEAT1 knockdown inhibited cell migration, enhanced epithelial barrier integrity, and reversed EMT-associated cytoskeletal remodeling. E-cadherin levels increased, while N-cadherin and vimentin decreased. Transcriptomic and functional analyses identified PAK4 as a NEAT1-regulated target. NEAT1 was shown to sponge miR-199-3p, thereby relieving its inhibitory effect on PAK4. Overexpression of miR-199-3p suppressed PAK4 and mitigated EMT-related changes induced by NEAT1. Conclusion: NEAT1 promotes EMT in nasal polyp epithelial cells by modulating the miR-199-3p/PAK4 axis, highlighting its potential as a diagnostic biomarker and therapeutic target in CRSwNP.

Indexed as

Epithelial-Mesenchymal TransitionMicroRNAsNasal Polypsp21-Activated KinasesRNA, Long NoncodingAnimalsCell LineCell MovementDisease Models, AnimalEpithelial CellsFemaleHumansMaleMiceMiddle AgedRhinitisMicroRNAsmirn199 microRNA, humanNEAT1 long non-coding RNA, humanp21-Activated KinasesPAK4 protein, humanRNA, Long NoncodingCRSwNPEMTmiR-199-3pNEAT1non-coding RNAPAK4

Identifiers

PMID40661947
PMCPMC12256258

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.