LINC00472 affects pancreatic β-cell function in type 2 diabetes mellitus by targeting miR-320b.

IF 3.2 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2026-04-03 DOI:10.1080/13813455.2026.2642259

Junli Li, Lin Yan, Huan Li, Lianjun Su, Jinfeng Fu

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引用次数: 0

Abstract

Objective: This study aimed to explore the role of LINC00472 in type 2 diabetes mellitus (T2DM).

Methods: Serum LINC00472 expression was detected in 34 patients with T2DM and 45 healthy controls via RT-qPCR, with ROC curve analysing its diagnostic value. Mouse pancreatic β-cell line INS-1 was induced with high glucose (HG) to establish HG-INS-1 model. si-LINC00472 and miR-320b inhibitor were transfected into HG-INS-1. CCK-8, flow cytometry, and ELISA kits were used to detect cell viability, apoptosis, insulin level, and oxidative stress indicators. Subcellular fractionation, dual-luciferase reporter, and RIP assays verified the interaction between LINC00472 and miR-320b.

Results: Serum LINC00472 was elevated in T2DM patients, with AUC = 0.882, 73.81% sensitivity, and 94.29% specificity. Silencing LINC00472 enhanced HG-INS-1 viability, reduced apoptosis, increased insulin, decreased ROS/MDA, and increased GSH. LINC00472 was mainly cytoplasmic and targeted miR-320b.

Conclusion: LINC00472 is a potential T2DM biomarker.

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LINC00472通过靶向miR-320b影响2型糖尿病胰腺β细胞功能。

目的：本研究旨在探讨LINC00472在2型糖尿病（T2DM）中的作用。方法：采用RT-qPCR检测34例T2DM患者和45例健康对照者血清中LINC00472的表达，并用ROC曲线分析其诊断价值。采用高糖（HG）诱导小鼠胰腺β细胞系INS-1建立ig -INS-1模型。将si-LINC00472和miR-320b inhibitor转染到HG-INS-1中。CCK-8、流式细胞术、ELISA检测细胞活力、凋亡、胰岛素水平、氧化应激指标。亚细胞分离、双荧光素酶报告基因和RIP实验验证了LINC00472和miR-320b之间的相互作用。结果：T2DM患者血清LINC00472升高，AUC = 0.882，敏感性73.81%，特异性94.29%。沉默LINC00472可增强HG-INS-1活性，减少细胞凋亡，增加胰岛素，降低ROS/MDA，增加GSH。LINC00472主要是细胞质的，靶向miR-320b。结论：LINC00472是一种潜在的T2DM生物标志物。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.