期刊文献+

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

Long noncoding RNA SLC26A4-AS1 inhibits proliferation and metastasis of breast cancer cells via Notch signaling pathway
下载PDF
导出
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5 cm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pcDNA3.1-SLC26A4-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。 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 5 cm 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 Notchl and Hesl 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 Notchl and Hesl in pcDNA3.1-SLC26A4-AS1 group were lower than pcDNA3.1 group(P<0.O1).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.
作者 姜春峰 张娜 邢鑫 张玉萍 宋蕾 JIANG Chunfeng;ZHANG Na;XING Xin;ZHANG Yuping;SONG Lei(Department of Interventional Oncology,Qingdao Central Hospital,Shandong,Oingdao 266042,China)
出处 《临床外科杂志》 2023年第9期834-837,共4页 Journal of Clinical Surgery
关键词 乳腺癌 SLC26A4-AS1 NOTCH1 HES1 breast cancer SLC26A4-AS1 Notchl Hesl
  • 相关文献

参考文献2

二级参考文献9

共引文献42

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部