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Updated: Sep 13, 2026

Immunofluorescent Labeling in Nasal Mucosa Tissue Sections of Allergic Rhinitis Rats via Multicolor Immunoassay
Published on: September 22, 2023
lncRNA DANCR Enhances Inflammatory Response in Allergic Rhinitis by Inhibiting miR-338-3p
Jinkai Han1, Bin Liu2, Yang Wang3
1Otolaryngology Head and Neck Surgery, Fu Yang People's Hospital, Fuyang, Anhui, China.
Abstract:
ObjectiveLong non-coding RNAs (lncRNAs) have been implicated in the development of allergic rhinitis (AR). This study aimed to examine the clinical importance and functional mechanism of lncRNA DANCR in AR.MethodsVolunteer participants, including healthy controls and those with AR, were recruited, with clinical information and serum samples being gathered. Expression of DANCR and miR-338-3p was quantified by qRT-PCR. An in vitro model of AR was established using IL-13-stimulated human nasal epithelial cells (HNECs), and modulation of target expression via molecular transfection was regulated. ELISA was used to measure IL-4, IL-5, eotaxin, and GM-CSF levels. Cell viability and apoptosis were assessed by CCK8 and flow cytometry, respectively. The interaction between DANCR and miR-338-3p was validated using a dual luciferase reporter system.ResultsSerum DANCR expression was significantly elevated in AR patients, showing high diagnostic accuracy (AUC = 0.878) with 82.05% sensitivity and 81.25% specificity. IL-13 stimulation increased DANCR in HNECs. IL-13 induction in HNECs led to an increase in inflammation, a decrease in cell viability, and modulation of apoptotic processes; however, silencing DANCR mitigated these IL-13-mediated effects. In AR and IL-13-induced HNECs, miR-338-3p was decreased, while DANCR functioned as its ceRNA. miR-338-3p silencing reversed the protective effects of DANCR downregulation.ConclusionIn this research, it was observed that elevated DANCR expression in AR was tightly linked to disease progression. Furthermore, it uncovered its mode of action in modulating inflammatory responses and cellular functions via miR-338-3p.