ArticleInternational journal of chronic obstructive pulmonary disease2025
A Peptide Encoded by lncRNA HOXB-AS3 Promotes Cigarette Smoke-Induced Inflammation in Bronchial Epithelial Cells via EZH2-Mediated H3K27me3 Modification.
Article in International journal of chronic obstructive pulmonary disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Epigenome-Wide Search for Distinctive Methylation Biomarkers of Endothelial and Leukocyte DNA.Epigenomes · 2025Article
- Epigenetic advances in rheumatic heart disease.Journal of translational autoimmunity · 2025Review
- m6A modification of non‑coding RNA: Mechanisms, functions and potential values in human diseases (Review).International journal of molecular medicine · 2025Review
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9 authors.
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Abstract
Background: Chronic obstructive pulmonary disease (COPD) primarily results from cigarette smoke (CS)-induced chronic inflammation. Although numerous long non-coding ribonucleic acids (lncRNAs) have been extensively studied for their crucial roles in COPD, the peptides encoded by these lncRNAs have garnered limited attention. This study aimed to investigate the role of a peptide encoded by lncRNA HOXB-AS3 in cigarette smoke extract (CSE)-induced inflammation and in 16HBE cells. Methods: Open reading frames (ORF) Find software was utilized to predict the encoding potential of HOXB-AS3. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect the levels of peptide HOXB-AS3-32aa in peripheral blood mononuclear cells (PBMCs) from both healthy controls and COPD patients and in 16HBE cells exposed to different CSE. To establish an in vitro inflammatory cell model of COPD, 16HBE cells were treated with 2% CSE. Enzyme-Linked Immunosorbent Assay (ELISA) measured inflammatory cytokines, while CCK-8 assay assessed cell viability. Flow cytometry was employed to assess cell apoptosis. Western blot analysis was performed to measure the expression of HOXB-AS3-32aa, EZH2, and H3K27me3 proteins. Co-Immunoprecipitation (Co-IP) was conducted to verify the interaction between EZH2 and HOXB-AS3-32aa. Results: Our findings revealed elevated expression of HOXB-AS3-32aa in PBMCs of COPD patients compared to controls. CSE treatment dose-dependently increased HOXB-AS3-32aa expression. Overexpression of HOXB-AS3-32aa exacerbated CS-induced inflammation in bronchial epithelial cells, leading to inhibited cell proliferation and increased cell apoptosis. Furthermore, HOXB-AS3-32aa suppressed EZH2 and H3k27me3 protein levels in 16HBE cells. Co-IP results confirmed the interaction between HOXB-AS3-32aa and EZH2 protein. Conclusion: Our results demonstrate that the novel peptide HOXB-AS3-32aa encoded by lncRNA HOXB-AS3 promotes CS-induced inflammation and apoptosis in 16HBE cells via EZH2-mediated H3K27me3 modification.
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