ArticleAmerican journal of translational research2022
Long non-coding RNA HOTTIP induces inflammation in asthma by promoting EFNA3 transcription by CCCTC-binding factor.
Article in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- The long antisense non-coding RNA HOXA transcript at the distal tip (LncRNA HOTTIP) in health and disease: a comprehensive review and in silico analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- LncRNA MEG3/CTCF-CXCR4 axis functions in the regulation of breast cancer cell migration.Non-coding RNA research · 2025Article
- CDC167 exhibits potential as a biomarker for airway inflammation in asthma.Mammalian genome : official journal of the International Mammalian Genome Society · 2024Article
- LncRNA HOTTIP as a diagnostic biomarker for acute respiratory distress syndrome in patients with sepsis and to predict the short-term clinical outcome: a case-control study.BMC anesthesiology · 2024Article
- Review
- Comprehensive analysis of immune-related genes for classification and immune microenvironment of asthma.American journal of translational research · 2023Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveLong non-coding RNAs (lncRNAs) function as vital regulators in biologic processes and are dysregulated in various tumors; however, little is known about their role in the inflammatory response in asthma. Therefore, this study aimed to investigate the function of antisense HOXA terminal transcriptional RNA (HOTTIP) and its possible mechanism in the ovalbumin (OVA)-induced inflammatory response in asthmatic mice.
methodsAsthma-related data resources from the Gene Expression Omnibus (GEO) database were extracted to explore the relationships between lncRNAs and asthma, and the lncRNA HOTTIP was identified. The probable effect of HOTTIP on airway inflammation was elaborated by ELISA and histopathologic analysis in OVA-sensitized mice. The online database excavation combined with RNA pull-down, RNA immunoprecipitation, luciferase reporter gene assay, and chromatin immunoprecipitation assay were used to analyze the targeted regulation relationship among HOTTIP, CCCTC-binding factor (CTCF), and Ephrin A3 (EFNA3). In addition,
resultsHOTTIP was upregulated in asthmatic mice and downregulating HOTTIP in the mice model of asthma markedly reduced inflammation, and caused less infiltration of inflammatory cells, and secretions of IgE, interleukin (IL)-4, IL-5, and IL-13. Mechanistically, the data indicate that HOTTIP promoted EFNA3 transcription by recruiting CTCF to the EFNA3 promoter. Interestingly, the knockdown of EFNA3 alleviated inflammation in the asthma model.
conclusionHOTTIP facilitates the airway inflammatory response by regulating EFNA3 transcription, providing a therapeutic target for asthma.
Indexed as
Identifiers
36628218PMC9827298W4315620668What OpenQuestion holds
Registered trials
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