已经记录了长链非编码RNA在胰腺癌（PC）进展中的重要性。在这里，我们鉴定了一种新的长链非编码RNA MIR600HG，并研究了它在PC进展中的潜在机制。通过生物信息学分析，我们选定了MIR600HG、miR-125a-5p和线粒体肿瘤抑制基因1（MTUS1）作为研究对象，并检测它们在收集的PC组织和PC细胞中的表达模式。通过在体内和体外操纵MIR600HG、miR-125a-5p和/或MTUS1，检测了胰腺癌细胞的生物学过程和肿瘤发生情况。结果表明，MIR600HG和MTUS1的水平在PC组织和细胞中下调，而miR-125a-5p则上调。MIR600HG可以与miR-125a-5p结合，而miR-125a-5p则可以负向作用于MTUS1。MIR600HG可抑制PC的恶性特性。miR-125a-5p升高可以逆转所有这些变化。此外，miR-125a-5p靶向MTUS1以激活胞外调节蛋白激酶信号通路。体内实验证实了MIR600HG在抑制PC方面的作用。总之，MIR600HG通过上调miR-125a-5p介导的MTUS1来抑制PC的进展，其中涉及胞外调节蛋白激酶信号通路。版权所有©2023 Wolters Kluwer Health, Inc.。保留所有权利。

Significance of long noncoding RNAs in pancreatic cancer (PC) progression has been documented. Here, we identified a novel long noncoding RNA MIR600HG in PC and its underlying mechanism during PC progression.Through bioinformatics analysis, we selected MIR600HG, microRNA-125a-5p (miR-125a-5p), and mitochondrial tumor suppressor 1 (MTUS1) as objects with their expression patterns assayed in the collected PC tissues and PC cells. Pancreatic cancer cells were manipulated with ectopic expression and deficiency of MIR600HG, miR-125a-5p, and/or MTUS1 for assaying cell biological processes in vitro and tumorigenesis in vivo.MIR600HG and MTUS1 levels were downregulated and miR-125a-5p was upregulated in PC tissues and cells. MIR600HG could bind to miR-125a-5p, while miR-125a-5p negatively targeted MTUS1. MIR600HG resulted in suppression in malignant properties of PCs. All these changes could be reversed by miR-125a-5p elevation. In addition, miR-125a-5p targeted MTUS1 to activate the extracellular regulated protein kinases signaling pathway. In vivo experiment also verified the inhibitory role of MIR600HG in PC.Taken together, MIR600HG acts as an inhibitor for PC progression by upregulating miR-125a-5p-mediated MTUS1 through extracellular regulated protein kinases pathway.Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.