Suppr超能文献

微小RNA-23a-3p通过抑制NDRG4的表达促进结肠癌的发展。

miR-23a-3p promotes the development of colon cancer by inhibiting the expression of NDRG4.

作者信息

Zuo Hao, Liu Shiqi, Li Xiangwei, Hou Guowei

机构信息

Department of General Surgery, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, No.1 Huanghe Xi Road, Huaian, 223300, Jiangsu, China.

出版信息

Clin Transl Oncol. 2023 Apr;25(4):933-940. doi: 10.1007/s12094-022-02996-4. Epub 2022 Nov 14.

Abstract

PURPOSE

Previous studies have found that miR-23a-3p, a diagnostic marker for colon cancer (CC), is upregulated in primary CC from stage I/II patients. Nevertheless, the specific functions and molecular mechanisms of miR-23a-3p in colon cancer remain unclear.

METHODS

The expression levels of miR-23a-3p and NDRG4 were analyzed by western blot and RT‒qPCR assays. Cell viability and proliferation were measured by CCK8 and colony formation assays. Cell apoptosis was assessed by flow cytometry. Cell migration and invasion were detected by transwell assay. Target binding was detected by luciferase reporter assay.

RESULTS

miR-23a-3p was dramatically elevated in CC tissues and cells. In HT29 and SW480 cells, downregulation of miR-23a-3p hampered cell proliferation, migration, and invasion while increasing cell apoptosis. The effects of miR-23a-3p silencing on CC progression were slowed by NDRG4 downregulation.

CONCLUSIONS

miR-23a-3p promoted CC progression by modulating the expression of NDRG4. This study demonstrated the mechanism of miR-23a-3p in CC, which may offer a new target for CC therapy.

摘要

目的

先前的研究发现,miR-23a-3p作为结肠癌(CC)的一种诊断标志物,在I/II期患者的原发性CC中表达上调。然而,miR-23a-3p在结肠癌中的具体功能和分子机制仍不清楚。

方法

通过蛋白质免疫印迹法和逆转录定量聚合酶链反应分析miR-23a-3p和NDRG4的表达水平。通过细胞计数试剂盒8法和集落形成试验检测细胞活力和增殖。通过流式细胞术评估细胞凋亡。通过Transwell试验检测细胞迁移和侵袭。通过荧光素酶报告基因试验检测靶标结合。

结果

miR-23a-3p在CC组织和细胞中显著升高。在HT29和SW480细胞中,miR-23a-3p的下调阻碍了细胞增殖、迁移和侵袭,同时增加了细胞凋亡。NDRG4的下调减缓了miR-23a-3p沉默对CC进展的影响。

结论

miR-23a-3p通过调节NDRG4的表达促进CC进展。本研究揭示了miR-23a-3p在CC中的作用机制,这可能为CC治疗提供新的靶点。

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