Suppr超能文献

长链非编码 RNA MIAT 促进腔 B 型乳腺癌细胞在体外的增殖、迁移和侵袭。

lncRNA MIAT promotes luminal B breast cancer cell proliferation, migration, and invasion in vitro.

机构信息

Molecular Immunology, College of Medical Technology, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, Sichuan, China.

Department of Breast Surgery, People's Hospital of Deyang City, Deyang, 618000, Sichuan, China.

出版信息

J Appl Genet. 2024 May;65(2):309-319. doi: 10.1007/s13353-023-00807-2. Epub 2023 Nov 21.

Abstract

Long noncoding RNAs (lncRNAs) play a role in the emergence and progression of several human tumors, including luminal B breast cancer (BC). The biological functions and potential mechanisms of lncRNA myocardial infarction-associated transcripts (MIAT) in luminal B BC, on the contrary, are unknown. In this work, we used UALCAN database analysis to find high expression of lncRNA MIAT in luminal BC tissues and also confirmed high levels of lncRNA MIAT expression in luminal B BC tissues and cells. In vitro knockdown of MIAT inhibited the proliferation, migration, and invasion of BT474 cells. In addition, we found that miR-150-5p levels were significantly reduced in luminal B BC specimens and cells, and miR-150-5p levels were significantly increased when MIAT was knocked down. And TIMER database analysis showed that MIAT was positively associated with PDL1. Through bioinformatic tools and in vitro experiments, lncRNA MIAT could function as a competitive endogenous RNA (CeRNA) to further regulate programmed cell death ligand 1 (PDL1) expression by directly sponging miR-150-5p. In conclusion, our data suggest that MIAT, an oncogene, may sponge miR-150-5p to regulate PDL1 expression and affect proliferation, migration, and invasion in luminal B BC in vitro.

摘要

长链非编码 RNA(lncRNA)在几种人类肿瘤的发生和发展中发挥作用,包括腔 B 型乳腺癌(BC)。相反,lncRNA 心肌梗塞相关转录物(MIAT)在腔 B BC 中的生物学功能和潜在机制尚不清楚。在这项工作中,我们使用 UALCAN 数据库分析发现 lncRNA MIAT 在腔 BC 组织中高表达,并在腔 B BC 组织和细胞中也证实了 lncRNA MIAT 的高水平表达。体外敲低 MIAT 抑制 BT474 细胞的增殖、迁移和侵袭。此外,我们发现 MIAT 在腔 B BC 标本和细胞中的水平显著降低,而当 MIAT 被敲低时,miR-150-5p 的水平显著增加。并且 TIMER 数据库分析表明 MIAT 与 PDL1 呈正相关。通过生物信息学工具和体外实验,lncRNA MIAT 可以作为竞争性内源 RNA(CeRNA),通过直接海绵 miR-150-5p 来进一步调节程序性细胞死亡配体 1(PDL1)的表达。总之,我们的数据表明,癌基因 MIAT 可能通过海绵 miR-150-5p 来调节 PDL1 的表达,并影响体外腔 B BC 的增殖、迁移和侵袭。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验