Evidence map›Paper›PMID 33785041›Full record

ArticleDiagnostic pathology2021

Let-7a-5p regulates the inflammatory response in chronic rhinosinusitis with nasal polyps.

Jianwei Zhang, Lei Han, Feng Chen

Open access · goldAbstract read
In one paragraph

Article in Diagnostic pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  3. Potential roles of microRNAs in chronic rhinosinusitis: from mechanistic insights to clinical studies.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 · 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

3 authors at 3 institutions in 1 country.

Jianwei Zhang *Department of Otolaryngology-Head and Neck Surgery, Shanghai Pudong New District Gongli Hospital/Second Military Medical University Affiliated Hospital, Shanghai, 200135, China.
Lei Han *Department of Otolaryngology-Head and Neck Surgery, Suqian First People's Hospital, The Suqian Clinical college of Xuzhou Medical University, Suqian, 223800, Jiangsu Province, China.
Feng ChenDepartment of Otorhinolaryngology-Head and Neck Surgery/ Research Institution of Otorhinolaryngology, Nanjing Drum Tower Hospital (The Affiliated Hospital of Nanjing University Medical School), Nanjing, 210008, Jiangsu Province, China. wunyovqgs403776@163.com.
Nanjing Drum Tower Hospital · CNSecond Military Medical University · CNXuzhou Medical College · CN

Funding

Key Disciplines Group Construction Project of Pudong Health Bureau of Shanghai PWZxq2017-04Key Specialty Construction Project of Health Bureau of Shanghai ZK2019C06Research Grant for Health Science and Technology of Pudong Health Bureau of Shanghai PW2019D-4
6 · The paper itself

Abstract

backgroundLet-7a-5p is demonstrated to be a tumor inhibitor in nasopharyngeal carcinoma. However, the role of let-7a-5p in chronic rhinosinusitis with nasal polyps (CRSwNP) has not been reported. This study is designed to determine the pattern of expression and role of let-7a-5p in CRSwNP.

methodsThe expression level of let-7a-5p, TNF-α, IL-1β, and IL-6 in CRSwNP tissues and cells were detected by RT-qPCR. Western blot assay was carried out to measure the protein expression of the Ras-MAPK pathway. Dual luciferase reporter assay and RNA pull-down assay were used to explore the relationship between let-7a-5p and IL-6.

resultsLet-7a-5p was significantly downregulated in CRSwNP tissues and cells. Moreover, the mRNA expression of TNF-α, IL-1β and IL-6 was increased in CRSwNP tissues, while let-7a-5p mimic inhibited the expression of TNF-α, IL-1β and IL-6. Besides that, let-7a-5p was negatively correlated with TNF-α, IL-1β and IL-6 in CRSwNP tissues. In our study, IL-6 was found to be a target gene of let-7a-5p. Additionally, let-7-5p mimic obviously reduced the protein levels of Ras, p-Raf1, p-MEK1 and p-ERK1/2, while IL-6 overexpression destroyed the inhibitory effect of let-7a-5p on the Ras-MAPK pathway in CRSwNP.

conclusionWe demonstrated that let-7a-5p/IL-6 interaction regulated the inflammatory response through the Ras-MAPK pathway in CRSwNP.

Indexed as

Cells, CulturedChronic DiseaseFemaleHumansInflammation MediatorsInterleukin-1betaInterleukin-6MaleMAP Kinase Kinase 1MicroRNAsMiddle AgedMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Nasal PolypsPhosphorylationProto-Oncogene Proteins c-rafIL1B protein, humanIL6 protein, humanInflammation MediatorsInterleukin-1betaInterleukin-6MAP2K1 protein, humanMAPK1 protein, humanMAPK3 protein, humanMAP Kinase Kinase 1MicroRNAsmirnlet7 microRNA, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-rafRaf1 protein, humanras ProteinsTNF protein, humanTumor Necrosis Factor-alphaChronic rhinosinusitis with nasal polypsIL-6Inflammatory responseLet-7a-5pRas-MAPK

Identifiers

PMID33785041
PMCPMC8008551
OpenAlexW3147526302

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.