Long non-coding RNA SNHG1 predicts disease severity of acute pancreatitis and stimulates pancreatic cell apoptosis and inflammatory response

急性胰腺炎 细胞凋亡 炎症反应 胰腺炎 炎症 长非编码RNA 疾病 医学 核糖核酸 细胞 癌症研究 内科学 免疫学 生物 基因 遗传学
作者
Zhuo Chen,Shengnan Liu,Sheng Wang,Yang Chen
出处
期刊:Journal of Environmental Pathology Toxicology and Oncology [Begell House Inc.]
卷期号:43 (4): 81-93
标识
DOI:10.1615/jenvironpatholtoxicoloncol.2024053229
摘要

Acute pancreatitis (AP) is a common digestive emergency, needs early prediction and recognition. The study examined the clinical value of long non-coding RNA SNHG1 in AP, and explored its related mechanism for AP. A total of 288 AP cases and 150 healthy persons were recruited, the AP patients were grouped based on AP severity. AR42J cells were treated with 100nM caerulein to stimulate AP in vitro. qRT-PCR was performed for mRNA detection. Receiver operating characteristic (ROC) curve was drawn for diagnostic significance evaluation. The relationship of SNHG1 and miR-140-3p was verified via luciferase reporter and RNA immunoprecipitation (RIP) assay. AP cases had high expression of SNHG1, and it can differentiate AP cases from healthy people with the area under the curve (AUC) of 0.899. Severe AP cases had high values of SNHG1, which was independently related to AP severity. SNHG1 knockdown relieved caerulein-induced AR42J cell apoptosis and inflammatory response. miR-140-3p interacted with SNHG1, and reversed the role of SNHG1 in caerulein-induced AR42J cell injury. RAB21 was a candidate target of miR-140-3p, and was at high expression in AP cell models. SNHG1 may be a promising biomarker for the detection of AP, and serves as a potential biological marker for further risk stratification in the management of AP. SNHG1 knockdown can relieve inflammatory responses and pancreatic cell apoptosis by absorbing miR-140-3p.
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