ArticleOncology letters2021
Long non-coding maternally expressed gene 3 regulates cigarette smoke extract-induced apoptosis, inflammation and cytotoxicity by sponging miR-181a-2-3p in 16HBE cells.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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.
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Who cites it
9 citing papers in PubMed, 24 citations in OpenAlex.
- GCBRGCN: Integration of ceRNA and RGCN to Identify Gastric Cancer Biomarkers.Bioengineering (Basel, Switzerland) · 2025Article
- Long non-coding RNA Small Nucleolar RNA Host Gene 4 ameliorates cigarette smoke-induced proliferation, apoptosis, inflammation, and airway remodeling in alveolar epithelial cells through the modulation of the mitogen-activated protein kinase signaling pathway via the microRNA-409-3p/Four and a Half LIM Domains 1 axis.European journal of medical research · 2024Article
- Article
- Interaction between long noncoding RNA and microRNA in lung inflammatory diseases.Immunity, inflammation and disease · 2024Review
- LncRNA PVT1 induces apoptosis and inflammatory response of bronchial epithelial cells by regulating miR-30b-5p/BCL2L11 axis in COPD.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023Article
- MEG3 Regulates CSE-Induced Apoptosis by Regulating miR-421/DFFB Signal Axis.International journal of chronic obstructive pulmonary disease · 2023Article
- LncRNA RP11-521C20.3 Inhibits Cigarette Smoke Extract-Induced Apoptosis in A549 Cells by Targeting BMF Signaling.International journal of chronic obstructive pulmonary disease · 2023Article
- XIST promotes apoptosis and the inflammatory response in CSE-stimulated cells via the miR-200c-3p/EGR3 axis.BMC pulmonary medicine · 2021Article
- MicroRNA 181a-2-3p Alleviates the Apoptosis of Renal Tubular Epithelial Cells via Targeting GJB2 in Sepsis-Induced Acute Kidney Injury.Molecular and cellular biology · 2021Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence has suggested that long non-coding (lnc)RNAs are widely involved in the progression of multiple diseases, including chronic obstructive pulmonary disease (COPD). The aim of the present study was to explore the function and molecule mechanism of maternally expressed gene 3 (MEG3) in cigarette smoke extract (CSE)-treated 16HBE cells. Cell viability and apoptosis were evaluated using Cell Counting Kit-8 analysis and flow cytometry, respectively. Western blot analysis was carried out to determine the protein levels of Bcl-2, Bax and cleaved caspase-3. ELISA assays were utilized to measure the protein levels of IL-1β and IL-6 and TNF-α. Cytotoxicity was assessed using a lactate dehydrogenase release assay. The expression levels of MEG3 and microRNA (miR)-181a-2-3p were detected using reverse transcription-quantitative PCR. The interaction between miR-181a-2-3p and MEG3 was predicted using DIANA tools and verified by a dual-luciferase reporter assay and RNA Immunoprecipitation assay. MEG3 expression was enhanced while miR-181a-2-3p abundance was reduced in the serum of patients with COPD and CSE-treated 16HBE cells. MEG3-knockdown or miR-181a-2-3p-overexpression inhibited CSE-induced apoptosis, inflammation and cytotoxicity in 16HBE cells. Moreover, miR-181a-2-3p directly bind to MEG3 and its knockdown reversed the inhibitory effect of MEG3 interference on apoptosis, inflammation and cytotoxicity in CSE-treated 16HBE cells. Overall, MEG3-knockdown suppressed CSE-induced apoptosis, inflammation and cytotoxicity in 16HBE cells by upregulating miR-181a-2-3p, providing a promising therapeutic target for treatment of CSE-induced COPD.
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Registered trials
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