肿瘤(癌症)患者之家
首页
癌症知识
肿瘤中医药治疗
肿瘤药膳
肿瘤治疗技术
前沿资讯
临床试验招募
登录/注册
VIP特权
广告
广告加载中...

文章:

miR-486-5p在结直肠癌干细胞表型中的作用

The Role of miR-486-5p on CSCs Phenotypes in Colorectal Cancer

原文发布日期:19 December 2024

DOI: 10.3390/cancers16244237

类型: Article

开放获取: 是

 

英文摘要:

Background: Colorectal cancer (CRC) is the third diagnosed cancer worldwide. Forty-four percent of metastatic colorectal cancer patients were diagnosed at an early stage. Despite curative resection, approximately 40% of patients will develop metastases within a few years. Previous studies indicate the presence of cancer stem cells (CSCs) and their contribution to CRC progression and metastasis. miRNAs deregulation plays a role in CSCs formation and in tumor development. In light of previous studies, we investigated the role of miR-486-5p to understand its role in CSC better. Methods: The expression of miR-486-5p was assessed in adherent cells and spheres generated from two CRC cell lines to observe the difference in expression in CSC-enriched spheroids. Afterward, we overexpressed and underexpressed this miRNA in adherent and sphere cultures through the transfection of a miR-486-5p mimic and a mimic inhibitor. Results: The results demonstrated that miR-486-5p exhibited a notable downregulation in CSC models, and its overexpression led to a significant decrease in colony size. Conclusions: In this study, we confirmed that miR-486-5p plays an oncosuppressive role in CRC, thereby advancing our understanding of the role of this microRNA in the CSC phenotype.

 

摘要翻译: 

背景:结直肠癌是全球第三大确诊癌症。44%的转移性结直肠癌患者在早期阶段被确诊。尽管进行了根治性切除,约40%的患者仍会在数年内发生转移。既往研究表明癌症干细胞的存在及其对结直肠癌进展和转移的促进作用,而miRNA表达失调在癌症干细胞形成及肿瘤发展中具有重要作用。基于前期研究,我们深入探讨miR-486-5p的作用机制以更好地理解其在癌症干细胞中的功能。方法:通过检测两种结直肠癌细胞系贴壁细胞与肿瘤球中miR-486-5p的表达水平,观察该miRNA在富集癌症干细胞的球状培养模型中的表达差异。随后通过转染miR-486-5p模拟物及其抑制剂,分别在贴壁培养和球状培养体系中实现该miRNA的过表达与低表达。结果:实验数据显示miR-486-5p在癌症干细胞模型中呈现显著下调,其过表达导致细胞集落尺寸明显减小。结论:本研究证实miR-486-5p在结直肠癌中发挥肿瘤抑制作用,从而深化了我们对这一微小RNA在癌症干细胞表型中作用机制的理解。

 

原文链接:

The Role of miR-486-5p on CSCs Phenotypes in Colorectal Cancer

广告
广告加载中...