ArticleJournal of molecular medicine (Berlin, Germany)2016
miR-26a suppresses EMT by disrupting the Lin28B/let-7d axis: potential cross-talks among miRNAs in IPF.
Article in Journal of molecular medicine (Berlin, Germany), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- A systematic review of overlapping microRNA patterns in systemic sclerosis and idiopathic pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2017Pooled it
- Bayesian Integration of Bronchoalveolar Lavage miRNAs and KL-6 in Progressive Pulmonary Fibrosis Diagnosis.Diagnostics (Basel, Switzerland) · 2025Article
- Circulating MicroRNAs in Idiopathic Pulmonary Fibrosis: A Narrative Review.Current issues in molecular biology · 2024Review
- The Role of lncRNA-miR-26a-mRNA Network in Cancer Progression and Treatment.Biochemical genetics · 2024Review
- MicroRNA-26a in respiratory diseases: mechanisms and therapeutic potential.Molecular biology reports · 2024Review
- LncRNA SNHG8 upregulates MUC5B to induce idiopathic pulmonary fibrosis progression by targeting miR-4701-5p.Heliyon · 2024Article
- Revisiting the role of MicroRNAs in the pathogenesis of idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Review
- Regulation of idiopathic pulmonary fibrosis: a cross-talk between TGF-Frontiers in medicine · 2024Review
- Metformin regulates the LIN28B‑mediated JNK/STAT3 signaling pathway through miR‑140‑3p in subretinal fibrosis.Experimental and therapeutic medicine · 2023Article
- Delivery of anti-microRNA-21 by lung-targeted liposomes for pulmonary fibrosis treatment.Molecular therapy. Nucleic acids · 2023Article
- Exosomal Micro-RNAs as Intercellular Communicators in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2022Review
- MiRNAs in Systemic Sclerosis Patients with Pulmonary Arterial Hypertension: Markers and Effectors.Biomedicines · 2022Article
- Exosomes in pathogenesis, diagnosis, and treatment of pulmonary fibrosis.Frontiers in pharmacology · 2022Review
- Downregulation of exosomal let-7d and miR-16 in idiopathic pulmonary fibrosis.BMC pulmonary medicine · 2021Article
- microRNA-186 in extracellular vesicles from bone marrow mesenchymal stem cells alleviates idiopathic pulmonary fibrosis via interaction with SOX4 and DKK1.Stem cell research & therapy · 2021Article
- Role of Non-Coding RNAs in Post-Transcriptional Regulation of Lung Diseases.Frontiers in genetics · 2021Review
- The function of non-coding RNAs in idiopathic pulmonary fibrosis.Open medicine (Warsaw, Poland) · 2021Review
- Lin28a attenuates TGF-β-induced renal fibrosis.BMB reports · 2020Article
- Decrypting the crosstalk of noncoding RNAs in the progression of IPF.Molecular biology reports · 2020Review
- The Epithelial-to-Mesenchymal Transition as a Possible Therapeutic Target in Fibrotic Disorders.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledIdiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and highly lethal fibrotic lung disease with unknown cause or cure. Although some microRNAs (miRNAs), such as miR-26a and let-7d, have been confirmed, the contribution to the pathophysiological processes of IPF, the roles of miRNAs and intrinsic links between them in fibrotic lung diseases are not yet well understood. In this study, we found that Lin28B could induce the process of epithelial-mesenchymal transition (EMT) by inhibiting let-7d, whereas inhibition of Lin28B mitigated TGF-β1-induced fibrogenesis and attenuated EMT in both cultured A549 cells and MLE-12 cells. More importantly, over-expression of miR-26a could simultaneously enhance the expression of let-7d in A549 cells, and further study confirmed that Lin28B was one of the direct targets of miR-26a, which mediates, at least in part, the regulatory effects of miR-26a on the biogenesis of let-7d. Finally, we constructed a regulatory network among miRNAs involved in the progression of IPF. Taken together, our study deciphered the essential role of Lin28B in the pathogenesis of EMT, and unraveled a novel mechanism that miR-26a is a modulator of let-7d. This study also defines the miRNAs network involved in IPF, which may have implications for developing new strategies for pulmonary fibrosis. KEY MESSAGE: Upregulation of Lin28B contributes to idiopathic pulmonary fibrosis. Lin28B causes epithelial-mesenchymal transition (EMT) by inhibition of let-7d. Lin28B is one of the targets of microRNA-26a. miR-26a enhances the expression of let-7d via targeting regulation of Lin28B. A regulatory network among miRNAs involved in the progression of IPF.
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Registered trials
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.