Suppr超能文献

长链非编码 RNA OIP5-AS1 通过靶向 miR-422a/ANO1 轴促进胃癌细胞生长。

LncRNA OIP5-AS1 facilitates gastric cancer cell growth by targeting the miR-422a/ANO1 axis.

机构信息

Department of General Surgery, Nanhua Hospital Affiliated to Nanhua University, Hengyang 421002, China.

出版信息

Acta Biochim Biophys Sin (Shanghai). 2020 Apr 20;52(4):430-438. doi: 10.1093/abbs/gmaa012.

Abstract

OPA-interacting protein 5 antisense transcript 1 (OIP5-AS1) plays an important regulatory role in various types of cancers. However, the functional role and regulatory mechanisms of OIP5-AS1 in gastric cancer (GC) remain largely unknown. In this study, we found that the expression of OIP5-AS1 was increased in GC tissues compared with that in adjacent non-cancerous tissues, which was significantly associated with shorter overall survival time of patients. In addition, OIP5-AS1 expression was also increased in GC cell lines including NCI-N87, MKN-45, BGC-823 and SGC-7901, when compared with that in normal gastric epithelial cell line GES-1. Knockdown of OIP5-AS1 markedly suppressed the proliferation and colony formation activities of GC cells, induced G0/G1 arrest and apoptosis of GC cells in vitro, and restrained tumor growth in vivo. Mechanistically, OIP5-AS1 functions as an oncogenic competing endogenous RNA by binding to and sequestering miR-422a to elevate the expression of anoctamin-1. Our study first demonstrated that OIP5-AS1 is a critical and powerful regulator of GC pathogenesis and may represent a novel candidate target for GC therapy.

摘要

OPA 相互作用蛋白 5 反义转录本 1(OIP5-AS1)在多种类型的癌症中发挥着重要的调节作用。然而,OIP5-AS1 在胃癌(GC)中的功能作用和调控机制在很大程度上仍不清楚。在本研究中,我们发现 OIP5-AS1 在 GC 组织中的表达高于相邻的非癌组织,这与患者的总生存时间明显相关。此外,与正常胃上皮细胞系 GES-1 相比,OIP5-AS1 在 GC 细胞系 NCI-N87、MKN-45、BGC-823 和 SGC-7901 中的表达也增加了。敲低 OIP5-AS1 可显著抑制 GC 细胞的增殖和集落形成活性,诱导 GC 细胞体外 G0/G1 期阻滞和凋亡,并抑制体内肿瘤生长。机制上,OIP5-AS1 作为一种致癌性竞争性内源 RNA,通过与 miR-422a 结合并将其隔离来提高 anoctamin-1 的表达。本研究首次证明 OIP5-AS1 是 GC 发病机制的关键和强大调节因子,可能代表 GC 治疗的新候选靶点。

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