miRNA-155及其靶基因在子宫内膜异位症中的生物学作用及分子机制  被引量:6

Molecular mechanism and biological function of miRNA-155 and its target genes on endometriosis

在线阅读下载全文

作  者:纪娜[1] 赵莉[1] 冯忻[1] 罗立梅[1] 梁婷[1] 庄晨玉 张丽华[1] 

机构地区:[1]南方医科大学中西医结合医院外四科,广东广州510315

出  处:《海南医学院学报》2015年第11期1463-1466,共4页Journal of Hainan Medical University

基  金:广东省中医药课题项目编号(2010222)~~

摘  要:目的:探讨miR-155及其靶基因在子宫内膜异位症(Ems)中的生物学作用及其分子机制研究。方法:RT-PCR检测miR-155在Ems患者和正常人中的表达。miR-155mimic和inhibtor转染到Ems中子宫内膜细胞中48h,通过MTT法检测细胞活力,transwell迁移和侵袭实验检测细胞迁移和侵袭能力,western blot检测细胞凋亡相关蛋白Bax、Bcl-2、基质金属蛋白酶(MMP 2)、MMP 9的表达。结果:Ems中miR-155表达高于正常子宫内膜,差异具有统计学意义(P<0.01)。Ems中子宫内膜细胞经miR-155mimic和inhibitor转染后,miR-155过表达显著提高细胞活力,抑制其凋亡,并促进细胞迁移侵袭,与下调Bax表达,上调Bcl-2、MMP 2及MMP 9表达有关。miR-155低表达作用相反。结论:miR-155低表达能抑制Ems中子宫内膜细胞的增生及迁移。Objective: To explore molecular mechanism and biological function of miR-155 and its target genes on endo- metriosis. Methods: The expression of miR-155 in endometriosis (Eros) patient and healthy control was assayed by RT-PCR. After miR-155 mimic and inhibtor were transfected into Ems endometrial cells for 48 h, the viability of cell was detected by MTT assay. Transwell migration and invasion assay were used to detect cell migration and invasion. The expression of cell apoptotic protein Bax and Bcl-2, matrix metalloproteinase (MMP 2) and MMP 9 was assayed by western blot. Results: The expression of miR-155 in Ems patient was more than that in health control (P〈0.01). After miR-155 mimic and inhibitor were transfected into Ems endometrial cells for 48 h, miR-155 over-expression could increase cell viability, and promote cell migration and invasion, which was related to down-regulation of Bax along with up-regulation of Bcl-2, MMP 2 and MMP 9. Conclusion: These results suggests that miR-155 lower expression can inhibit endometrial cell proliferation and migration of the Ems.

关 键 词:MIR-155 子宫内膜异位症 迁移 

分 类 号:R711.71[医药卫生—妇产科学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象