临床外科杂志 ›› 2023, Vol. 31 ›› Issue (9): 834-837.doi: 10.3969/j.issn.1005-6483.2023.09.010

• 论著 • 上一篇    下一篇

长链非编码RNA SLC26A4反义RNA 1通过Notch信号抑制乳腺癌细胞增殖与转移

  

  1. 266042 山东省青岛市中心医院肿瘤介入科  
  • 收稿日期:2023-01-31 出版日期:2023-09-20 发布日期:2023-09-20
  • 通讯作者: 宋蕾,Email:songlei777@126.com

Long noncoding RNA SLC26A4-AS1 inhibits proliferation and metastasis of breast cancer cells via Notch signaling pathway

  1. Department of Interventional Oncology,Qingdao Central Hospital,Shandong,Qingdao 266042, China
  • Received:2023-01-31 Online:2023-09-20 Published:2023-09-20

摘要: 目的 探讨长链非编码RNA(lncRNA)SLC26A4反义RNA 1(SLC26A4-AS1)在乳腺癌细胞增殖、迁移和侵袭中的作用及潜在生物学机制。方法 2017年6月~2020年12月乳腺癌组织及对应癌旁组织(距离癌组织边缘5cm以上)40例,采用实时荧光定量PCR(qRT-PCR)技术检测SLC26A4-AS1在乳腺癌组织和细胞系的表达。选择乳腺癌细胞MCF7作为研究对象,将细胞分为control组、pcDNA3.1组、pcDNA3.1-SLC26A4-AS1组和pcDNA3.1SLC26A4-AS1+Notch激动剂组。qRT-PCR检测SLC26A4-AS1对Notch信号通路中关键因子Notch1和Hes1表达的影响。MTT比色法、划痕实验和Transwell小室实验分别检测细胞增殖、迁移和侵袭能力。结果 SLC26A4-AS1在乳腺癌组织和细胞表达降低。pcDNA3.1-SLC26A4-AS1组Notch1和Hes1的表达量低于pcDNA3.1组,差异有统计学意义(P<0.01)。pcDNA3.1-SLC26A4-AS1组MCF7细胞活力、伤口愈合率和穿膜细胞数量均低于pcDNA3.1组,差异有统计学意义(P<0.01)。pcDNA3.1-SLC26A4-AS1+Notch激动剂组MCF7细胞活力、伤口愈合率和穿膜细胞数量均高于pcDNA3.1-SLC26A4-AS1组,差异有统计学意义(P<0.01)。结论 SLC26A4-AS1在乳腺癌中表达下调,其过表达抑制乳腺癌细胞的增殖、迁移和侵袭。SLC26A4AS1参与抑制Notch信号通路活化提供了一种新的表观遗传学调控机制。

关键词: 乳腺癌, SLC26A4-AS1, Notch1, Hes1

Abstract: Objective To investigate the effects of long noncoding RNA(lncRNA) SLC26A4 antisense RNA 1(SLC26A4-AS1) on proliferation,migration and invasion of breast cancer cell and the underlying mechanisms. Methods From June 2017 to December 2020, there were 40 cases of breast cancer tissue and corresponding paracancer tissue (more than 5cm away from the margin of cancer tissue).The expression levels of SLC26A4-AS1 in breast cancer tissues and cell lines were determined by quantitative real-time PCR(qRT-PCR).MCF7 cell was selected and allocated into:control group,pcDNA3.1 group,pcDNA3.1-SLC26A4-AS1 group and pcDNA3.1-SLC26A4-AS1+Notch activator group.The effects of SLC26A4-AS1 on expressions of Notch1 and Hes1 in Notch signaling pathway were examined by qRT-PCR.Cell viability(Proliferation),migration and invasive were determined by MTT assay,Scratch and Transwell assay. Results SLC26A4-AS1 was significantly down-regulated in breast cancer tissues and cell lines.The expressions of Notch1 and Hes1 in pcDNA3.1-SLC26A4-AS1 group were lower than pcDNA3.1 group(P<0.01).The cell viability,wound healing rate and number of transmembrane cells of pcDNA3.1-SLC26A4-AS1 group were inhibited compared with pcDNA3.1 group(P<0.01).The cell viability,wound healing rate and number of transmembrane cells of pcDNA3.1-SLC26A4-AS1+Notch activator group were promoted compared with pcDNA3.1-SLC26A4-AS1 group(P<0.01). Conclusions SLC26A4-AS1 was down-regulated in breast cancer,and overexpression of SLC26A4-AS1 curtailed proliferation,migration and invasion of breast cancer cells.SLC26A4-AS1 provides a novel epigenetic mechanism involved in deactivation of Notch signaling pathway.

Key words: breast cancer, SLC26A4-AS1, Notch1, Hes1

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