基因沉默
细胞凋亡
免疫学
流式细胞术
炎症
转染
生物
下调和上调
刺激
免疫系统
体外
癌症研究
活力测定
细胞培养
医学
报告基因
细胞
细胞生长
实时聚合酶链反应
基因表达
促炎细胞因子
内生
体内
信使核糖核酸
过敏性炎症
基因表达调控
作者
Jinkai Han,Bin Liu,Yang Wang,Ning Li
标识
DOI:10.1177/19458924261484683
摘要
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI