Evidence map›Paper›PMID 39472569›Full record

ArticleScientific reports2024

LncRNA FEZF1-AS1 promotes pulmonary fibrosis via up-regulating EZH2 and targeting miR-200c-3p to regulate the ZEB1 pathway.

Mengmeng Liu, Longfei Song, Yuxin Lai, Fusheng Gao, Jun Man

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
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  5. Review
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  7. 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

5 authors.

Mengmeng LiuDepartment of Clinical Laboratory, Affiliated Hospital of Shandong Second Medical University, No. 2428, Yuhe Road, Kuiwen District, Weifang City, 261041, Shandong Province, China.
Longfei SongDepartment of Rehabilitation Medicine, Affiliated Hospital of Shandong Second Medical University, No. 2428 Yuhe Road, Kuiwen District, Weifang City, 261041, Shandong Province, China.
Yuxin LaiBeijing University of Chinese Medicine, No. 11 on North 3rd Ring Road, Beijing, 100029, China.
Fusheng GaoDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Shandong Second Medical University, No. 2428, Yuhe Road, Kuiwen District, Weifang City, 261041, Shandong Province, China. gaofs888@163.com.
Jun ManDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Shandong Second Medical University, No. 2428, Yuhe Road, Kuiwen District, Weifang City, 261041, Shandong Province, China. manjun0229@126.com.

Funding

Clinical research project of Affiliated Hospital of Weifang Medical College, Shandong Province, China 2022wyfylcyj05National Natural Science Foundation of China 82205079Natural Science Foundation of Shandong Province ZR2023QH061Weifang Municipal Health Commission Traditional Chinese Medicine Research Project WFZYY2024-4-004
6 · The paper itself

Abstract

The role and detailed mechanisms of lncRNAs in idiopathic pulmonary fibrosis (IPF) are not fully understood. qPCR was conducted to verify lncRNA FEZF1-AS1 expression in the transforming growth factor-beta 1 (TGF-β1)-stimulated human lung fibroblasts (HLF) and A549. The EMT-related proteins were performed by western blotting. Cell proliferation, migration, and transition were detected by CCK-8, colony formation, wound-healing and transwell assays. A dual-luciferase reporter assay was conducted to validate the target relationship of FEZF1-AS1 and miR-200c-3p. FEZF1-AS1 is highly expressed in the fibrotic A549 and HLF. in vitro experiments revealed that FEZF1-AS1 facilitates cell proliferation, migration and invasion. Knockdown of FEZF1-AS1 attenuated TGF-b1-induced fibrogenesis both in vitro. Moreover, silencing FEZF1-AS1 inhibited fibrogenesis through modulation of miR-200c-3p. In addition, inhibition of miR-200c-3p promoted fibrogenesis by regulation of Zinc finger E-box binding homeobox 1 (ZEB1). Mechanistically, FEZF1-AS1 promoted lung fibrosis by acting as a competing endogenous RNA (ceRNA) for miR-200c-3p. FEZF1-AS1 silencing increased the expression and activity of miR-200c-3p to inhibit ZEB1 and alleviate lung fibrogenesis in A549 and HLF. In addition, our study showed that FEZF1-AS1 can regulate enhancer of zeste homolog2 (EZH2) to upregulate fibrosis-related proteins and promote lung fibrosis. In summary, the results of our study revealed the pulmonary fibrogenic effect of FEZF1-AS1 in cellular experiments, demonstrating the potential roles and mechanisms of the FEZF1-AS1/miR-200c-3p/ZEB1 and FEZF1-AS1/EZH2 pathways, which provides a novel and potential therapeutic target to lung fibrosis.

Indexed as

Cell ProliferationEnhancer of Zeste Homolog 2 ProteinMicroRNAsRNA, Long NoncodingZinc Finger E-box-Binding Homeobox 1A549 CellsCell MovementEpithelial-Mesenchymal TransitionFibroblastsHumansPulmonary FibrosisRepressor ProteinsSignal TransductionTransforming Growth Factor beta1Up-RegulationEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanFEZF1 protein, humanMicroRNAsMIRN200 microRNA, humanRepressor ProteinsRNA, Long NoncodingTransforming Growth Factor beta1ZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1Enhancer of zeste homolog2 (EZH2)Fibrosis-related proteinsIdiopathic pulmonary fibrosis (IPF)LncRNA FEZF1-AS1miR-200c-3pZinc finger E-box binding homeobox 1 (ZEB1)

Identifiers

PMID39472569
PMCPMC11522518

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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 OpenQuestion graph.