ArticleOncology letters2017
Pirfenidone may revert the epithelial-to-mesenchymal transition in human lung adenocarcinoma.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Cannabidiol inhibits TGF-β1-induced epithelial-mesenchymal transition in human conjunctival epithelial cells by interrupting TGF-β/Smad signaling.Scientific reports · 2025Article
- The Role of Antifibrotic Therapy in Pulmonary Fibrosis and Lung Cancer: A Multicenter Retrospective Analysis.Biomedicines · 2025Article
- The unexplored mechanism of antitumoral effect of pirfenidone in melanoma cells.Scientific reports · 2025Article
- Huaxian formula alleviates nickel oxide nanoparticle-induced pulmonary fibrosis via PI3K/AKT signaling.Scientific reports · 2025Article
- Impact of antifibrotic therapy on lung cancer incidence and mortality in patients with idiopathic pulmonary fibrosis.Journal of thoracic disease · 2024Article
- The role of epithelial-mesenchymal transition in pulmonary fibrosis: lessons from idiopathic pulmonary fibrosis and COVID-19.Cell communication and signaling : CCS · 2024Review
- Modeling fibrotic alveolar transitional cells with pluripotent stem cell-derived alveolar organoids.Life science alliance · 2023Article
- A Cell-Fate Reprogramming Strategy Reverses Epithelial-to-Mesenchymal Transition of Lung Cancer Cells While Avoiding Hybrid States.Cancer research · 2023Article
- Phosphorylation of PHF2 by AMPK releases the repressive H3K9me2 and inhibits cancer metastasis.Signal transduction and targeted therapy · 2023Article
- Losartan enhances the suppressive effect of pirfenidone on the bleomycin-induced epithelial-mesenchymal transition and oxidative stress in A549 cell line.Iranian journal of basic medical sciences · 2023Article
- Lung cancer in patients with fibrosing interstitial lung diseases: an overview of current knowledge and challenges.ERJ open research · 2022Review
- Pirfenidone Sensitizes NCI-H460 Non-Small Cell Lung Cancer Cells to Paclitaxel and to a Combination of Paclitaxel with Carboplatin.International journal of molecular sciences · 2022Article
- The Invasion and Metastasis of Colon Adenocarcinoma (COAD) Induced by SALL4.Journal of immunology research · 2022Article
- Review
- Article
- Fibroblast Growth Factor 2 Augments Transforming Growth Factor Beta 1 Induced Epithelial-mesenchymal Transition in Lung Cell Culture Model.Iranian journal of allergy, asthma, and immunology · 2020Article
- Pirfenidone alleviates pulmonary fibrosis in vitro and in vivo through regulating Wnt/GSK-3β/β-catenin and TGF-β1/Smad2/3 signaling pathways.Molecular medicine (Cambridge, Mass.) · 2020Article
- Pirfenidone anti-fibrotic effects are partially mediated by the inhibition of MUC1 bioactivation.Oncotarget · 2020Article
- Proteomic analysis of anti-angiogenic effects by conbercept in the mice with oxygen induced retinopathy.International journal of ophthalmology · 2020Article
- Pirfenidone inhibits epithelial-mesenchymal transition in keloid keratinocytes.Burns & trauma · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial-to-mesenchymal transition (EMT) in cancer is associated with invasion, metastasis and chemoresistance. Recent studies have revealed the increased expression of programmed death-ligand 1 (PD-L1) in cells undergoing EMT. The underlying mechanism of EMT involves transforming growth factor-β (TGF-β) and fibroblast growth factor-2 (FGF-2). Pirfenidone and the known EMT-suppressor nintedanib suppress pulmonary fibrosis partially through suppression of TGF-β. The present study aimed to determine whether pirfenidone has the potential to induce EMT-reversion, using nintedanib as a reference. The human lung adenocarcinoma cell lines A-549, HCC-827, and PC-9 were treated with TGF-β and FGF-2 to induce EMT. The EMT-induced cells were further treated with pirfenidone or nintedanib. Phenotypic alterations associated with EMT were assessed by examining the following: i) The expression levels of E-cadherin, vimentin, fibronectin and slug, using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and fluorescent immunohistochemistry; ii) cell motility via wound-healing assays; and iii) the expression of PD-L1 using RT-qPCR. The combination of TGF-β and FGF-2 successfully induced EMT in all three cell lines, characterized by a significant reduction in E-cadherin expression in the A-549 and HCC-827 cells, increased expression levels of vimentin, fibronectin, slug and PD-L1, and increased cell motility in all three cell lines. Pirfenidone and nintedanib reverted all of these phenotypes, with the exception of unaltered E-cadherin expression in all three cell lines, and inconsistent expression of vimentin in the HCC-827 and PC-9 cells. Thus, pirfenidone and nintedanib have the ability to induce EMT-reversion in human lung adenocarcinoma.
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