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长链非编码 RNA MIR600HG 通过与 microRNA-125a-5p 结合，抑制细胞外调节蛋白激酶信号通路，从而依赖于线粒体肿瘤抑制因子 1 抑制胰腺癌细胞的进展。

Long Noncoding RNA MIR600HG Binds to MicroRNA-125a-5p to Prevent Pancreatic Cancer Progression Via Mitochondrial Tumor Suppressor 1-Dependent Suppression of Extracellular Regulated Protein Kinases Signaling Pathway.

机构信息

From the Intensive Care Unit, Affiliated Hospital of Zunyi Medical University.

Department of Medical Genetics, Zunyi Medical University, Zunyi, China.

出版信息

Pancreas. 2022;51(10):1434-1443. doi: 10.1097/MPA.0000000000002185.

DOI:10.1097/MPA.0000000000002185

PMID:37099789

Abstract

OBJECTIVES

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.

METHODS

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.

RESULTS

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.

CONCLUSIONS

Taken together, MIR600HG acts as an inhibitor for PC progression by upregulating miR-125a-5p-mediated MTUS1 through extracellular regulated protein kinases pathway.

摘要

目的

长链非编码 RNA 在胰腺癌（PC）进展中的意义已得到证实。在这里，我们鉴定了一种新型的长链非编码 RNA MIR600HG 在 PC 及其在 PC 进展过程中的潜在机制。

方法

通过生物信息学分析，我们选择 MIR600HG、microRNA-125a-5p（miR-125a-5p）和线粒体肿瘤抑制因子 1（MTUS1）作为研究对象，检测其在收集的 PC 组织和 PC 细胞中的表达模式。通过转染使胰腺癌细胞过表达和敲低 MIR600HG、miR-125a-5p 和/或 MTUS1，体外检测细胞生物学过程和体内肿瘤发生情况。

结果

MIR600HG 和 MTUS1 的水平在 PC 组织和细胞中下调，miR-125a-5p 上调。MIR600HG 可以与 miR-125a-5p 结合，而 miR-125a-5p 负向靶向 MTUS1。MIR600HG 导致胰腺癌细胞恶性特性的抑制。这些变化都可以通过 miR-125a-5p 的升高而逆转。此外，miR-125a-5p 通过激活细胞外调节蛋白激酶信号通路靶向 MTUS1。体内实验也验证了 MIR600HG 在 PC 中的抑制作用。