ArticleCell biology and toxicology2021
In vitro study of the role of FOXO transcription factors in regulating cigarette smoke extract-induced autophagy.
Article in Cell biology and toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Salvianolic Acid A Relieves Acute Lung Injury by Promoting the Expression of FOXO1 and Activating Autophagy Through the Inhibition of miR-217-5p.Biochemical genetics · 2026Article
- Protective Effects ofFood science & nutrition · 2026Article
- FOXO1 contributes to cigarette smoke condensate-induced cellular senescence and fibrosis in lung fibroblasts through activating the TGF-β1/Smad2/3 signaling pathway.Immunologic research · 2025Article
- Unraveling the Hsp70-ROS-autophagy axis in pentachlorophenol-challenged lung and liver epithelial cells.Archives of toxicology · 2025Article
- Transcriptomic profiles of single-cell autophagy-related genes (ATGs) in lung diseases.Cell biology and toxicology · 2025Article
- miRNA Signatures in Alveolar Macrophages Related to Cigarette Smoke: Assessment and Bioinformatics Analysis.International journal of molecular sciences · 2025Article
- Impact of exercise-induced DNA damage repair on age-related muscle weakness and sarcopenia.Frontiers in genetics · 2025Review
- Interplay between proteasome function and inflammatory responses in e-cig vapor condensate-challenged lung epithelial cells.Archives of toxicology · 2023Article
- Article
- Recent evidence from omic analysis for redox signalling and mitochondrial oxidative stress in COPD.Journal of inflammation (London, England) · 2022Review
- A Review of Toxicity Mechanism Studies of Electronic Cigarettes on Respiratory System.International journal of molecular sciences · 2022Review
- Cigarette Smoke Exposure Increases Glucose-6-phosphate Dehydrogenase, Autophagy, Fibrosis, and Senescence in Kidney CellsOxidative medicine and cellular longevity · 2022Article
- Associative analysis of multi-omics data indicates that acetylation modification is widely involved in cigarette smoke-induced chronic obstructive pulmonary disease.Frontiers in medicine · 2022Article
- Wenshen Yiqi Keli Mitigates the Proliferation and Migration of Cigarette Smoke Extract-Induced Human Airway Smooth Muscle Cells through miR-155/FoxO3a Axis.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- A cellular census of human peripheral immune cells identifies novel cell states in lung diseases.Clinical and translational medicine · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Cigarette smoking is the chief etiological factor for chronic obstructive pulmonary disease (COPD). Oxidative stress induced by cigarette smoke (CS) causes protein degradation, DNA damage, and cell death, thereby resulting in acute lung injury (ALI). In this regard, autophagy plays a critical role in regulating inflammatory responses by maintaining protein and organelle homeostasis and cellular viability. Expression of autophagy-related proteins (ARPs) is regulated by the fork head box class O (FOXO) transcription factors. In the current study, we examined the role of FOXO family proteins-FOXO1 and FOXO3a-in regulating CS extract (CSE)-induced autophagy. Using human lung adenocarcinoma cells with type II alveolar epithelial characteristics (A549), we observed CSE-mediated downregulation of FOXO3a. In contrast, there was a pronounced increase in the expression of FOXO1 at both the transcriptional and translational levels in the CSE-challenged cells compared with controls. Interestingly, knockdown of FOXO3a heightened the CSE-mediated increase in expression of cytokines/chemokines (IL-6, IL-8, and MCP-1), ARPs, and the FOXO1 transcription factor. Moreover, FOXO1 knockdown rescued CSE-mediated upregulation of ARPs in A549 cells. In addition, using the ROS inhibitor N-acetyl-L-cysteine (NAC), we observed abrogated mRNA expression of several ARPs and production of inflammatory cytokines/chemokines (IL-6, IL-8, MCP-1, and CCL-5) in the CSE-challenged cells suggesting an important role of ROS in regulating CSE-induced autophagy. Chromatin immunoprecipitation of FOXO1 and FOXO3a demonstrated increased binding of the former to promoter regions of autophagy genes- BECLIN1, ATG5, ATG12, ATG16, and LC3 in CSE challenged cells. These findings suggest the role of FOXO1 in regulating the expression of these genes during CSE exposure. Overall, our findings provide evidence for FOXO3a-dependent FOXO1-mediated regulation of autophagy in the CSE-challenged cells. Graphical abstract.
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